TruthArchive.ai - Tweets Saved By @dbdugger

Posted - August 18, 2025 at 10:20 AM

Saved - August 18, 2025 at 10:54 AM

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I reflect on the complexities of ME/CFS, noting that millions have sacrificed their cognition due to the effects of the Spike protein from both SARS-CoV-2 infections and vaccines. The persistence of Spike leads to serious health issues, including cognitive impairments akin to those seen in HIV-related conditions. Studies indicate a significant overlap between cognitive symptoms in COVID-19 and HIV-associated neurocognitive disorders. As we explore treatment options, understanding the long-term implications of Spike and its cumulative effects remains crucial for both adults and children.

@dbdugger - Daniel Brittain Dugger

We must accept "Solving ME/CFS" required sacrificing the cognition of millions, including those robbed of their cognition and autonomy after allowing conversion from Asymptomatic Neurocognitive Impairment.

@AnneliseBocquet - Bocquet Annelise 🔬🧬📚🚜

5 points fondamentaux que vous devez savoir sur la Spike du SARS-CoV-2 (🦠 et 💉) De retour après plusieurs jours de pause... et ça fait du bien ! Je lance ce thread en 5 points. 1. La Spike est produite aussi bien lors d'une infection par le SARS-CoV-2 que par les injections anti-covid. Si on a des données solides pour les covid-longs, on en a beaucoup moins pour les PVS (Syndromes Post-Vaccination). Les études sont disparates et il n'y a aucune étude comparative. Du moins, pas à ma connaissance. Ce que je sais, c'est que la Spike est potentiellement la responsable de ces PVS. Les injections anti-covid font produire de la Spike... mais en quelle quantité ? Et quid de la biodistribution - autrement dit, on n'a toujours aucune idée de la production de Spike dans les tissus. 2. La Spike enclenche divers problèmes : les Spikeopathies. De fait toxique, elle persiste dans les organismes pendant des mois... voir des ANNÉES. Et il y a donc un effet cumulatif. Du fait de sa persistance, la Spike des injections anti-covid vient se rajouter à la Spike des infections covid... créant un vrai problème de dose cumulative. Et une synergie "virus + injections anti-covid". Car oui, les injections anti-covid ne protègent pas, ni des infections ni des formes graves. Mais rajoutent de la Spike sur de la Spike. 3. La Spike est dégénérative. Elle est amyloides, amyloidogène et peut utiliser les fibres amyloides pour permettre au virus de coloniser l'organisme. On aura des pathologies comme Alzheimer, Parkinson, des démences et diverses des amyloses comme les fibrinaloides... (Creutzfeld Jakob) (Amyloses) 4. La Spike est toxique pour le système immunitaire. - du fait de sa persistance, elle peut épuiser les lymphocytes T. Là aussi, l'épuisement des lymphocytes T est un marqueur aussi bien des covid-longs que des PVS. Mais, du coup, qui dit "système immunitaire épuisé" dit "système immunitaire hors-service". C'est devenu une passoire pour les pathogènes... surtout le SARS-CoV-2. 5. La Spike entraîne des perturbations métaboliques... C'est en lien avec ses propriétés cancérigènes mais aussi, son impact sur l'ensemble de l'organisme. Fatigue chronique et perte du tonus musculaire sont deux grandes caractéristiques. Être spiké, c'est passer dans une essoreuse... avec des impacts de fond. Beaucoup de questions sont encore en suspens... comme les effets épigénétiques, les impacts sur les futures générations et la fertilité. Mais ces 5 points là sont déjà beaucoup d'arguments à opposer aux injections anti-covid et à demander aux soignants de... nous soigner. Le potentiel bacteriophage du SARS-CoV-2 est un argument clé en faveur des antibiotiques. Limiter la propagation du virus dans l'organisme et donc la production de Spike est important ! Fondamental au regard de la persistance de la protéine Spike et des Spikeopathies, des propriétés amyloides (et donc dégénératives), immunotoxiques et des impacts métaboliques. Cela vaut pour les adultes mais aussi les enfants. Merci beaucoup de m'avoir lue. 💯💯💯

@ejustin46 - Emmanuel

How many spike proteins are in our body during each SARS-CoV-2 infection, and how many stay in our organs after three infections? 500,000,000,000 spike proteins ? I haven't found a clear answer in the nearly 10,000 studies that I shared on X/Twitter since the pandemic began.

@AnneliseBocquet - Bocquet Annelise 🔬🧬📚🚜

Bien... un nouveau preprint. https://www.medrxiv.org/content/10.1101/2025.02.18.25322379v1 Voilà ce qu'en tant qu'immuno, je retiens... 1. Quelques définitions : 1.a. Post-Vaccination Syndrome (PVS) ou Syndrome Post-Vaccination (en français) : PVS fait référence à un ensemble de symptômes chroniques (fatigue,

Immunological and Antigenic Signatures Associated with Chronic Illnesses after COVID-19 Vaccination medRxiv - The Preprint Server for Health Sciences medrxiv.org

@AnneliseBocquet - Bocquet Annelise 🔬🧬📚🚜

Bon ben... ça y est... c'est publié ! La protéine Spike du SARS-CoV-2 s'accumule et persiste dans l'organisme pendant... DES ANNÉES ! Avec, notamment une accumulation dans le cerveau, les méninges et le crâne... C'est ce thread là qui vient d'être validé peer-reviewed ⤵️

@AnneliseBocquet - Bocquet Annelise 🔬🧬📚🚜

Bien... petite réaction à chaud sur cette publication de Nakao Ora et al. 2025. Persistance de la Spike dans les syndromes post-vaccinaux (PVS) Persistance de la Spike après infection par le SARS-CoV-2 et persistance du virus.

Video Transcript AI Summary

Cette vidéo résume: selon Nakaoota et al. (3 avril 2025), « l’expression de la protéine Spike chez 43.8 pour 100 des personnes vaccinées anti Covid » persiste « au niveau des artères coronaires » jusqu’à 17 mois après l’injection, avec « l’ARN messager, du vaccin, mais également du virus » détecté. Il y a « persistance de la protéine Spike » et « persistance du SARS-CoV-2 » possiblement malgré les traitements précoces. L’auteure mentionne aussi « Crüssfeld Jacob, 14 mois après infection » et une étude sur des « AVC 17 mois après injections ». L’interaction de la nucléocapside (protéine N) avec TRIM28 pourrait retarder la réponse immunitaire innée, renforçant la tolérance immunitaire via TLR2/RAGE et IgG4. Conséquences: infection potentiellement asymptomatique et dégâts cumulatifs; Spike persistante pourrait entraîner « spike viral plus spike vaccinal ». Des spycopathies neurologiques sont évoquées; dépistage de Spike et traque du virus recommandés; traitements personnalisés et soutien par curcumine, quercétine, vitamine D; approche individuelle. This video summarizes: according to Nakaoota et al. (April 3, 2025), « the expression of the spike protein in 43.8 per 100 of vaccinated people » persists « at the level of the coronary arteries » for up to 17 months after injection, with « mRNA from the vaccine, but also the virus » detected. There is « persistence of the Spike protein » and « persistence of SARS-CoV-2 » possibly despite early treatments. The author also cites « Crüssfeld Jacob, 14 months after infection » and a study on « strokes 17 months after injections ». The interaction of the nucleocapsid protein (N) with TRIM28 could delay the innate antiviral response, reinforcing immune tolerance via TLR2/RAGE and IgG4. Consequences: potentially asymptomatic infection and cumulative damage; persistent Spike could lead to « spike viral plus spike vaccinal ». Neurological spycopathies are discussed; diagnostics to detect Spike and tracking the virus are recommended; therapies to block/remove Spike and personalized approaches, with supports like curcumin, quercetin, vitamin D.

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Full Transcript

Speaker 0: Bonjour à tous et à tous. Je suis Annelies Bocket, je suis docteure en biologie santé et spécialisée en immunologie, et je n'ai absolument aucun conflit d'intérêt, que ce soit d'ordre privé, personnel, financier, peu importe. Je n'ai pas de conflit d'intérêt. Je me permets de faire cette petite vidéo suite à la parution d'un nouvel article de Nakaoota et al en date du 3 avril 2025 qui démontre l'expression de la protéine Spike chez 43.8 pour 100 des personnes vaccinées anti Covid avec une persistance de cette protéine Spike au niveau des artères coronaires et ce jusqu'à 17 mois après l'injection. On a également détecté de l'ARN messager, du vaccin, mais également du virus au niveau donc de ces artères coronaires. Donc il y a bien une persistance de la protéine Spike. Je ne reviendrai pas sur l'étude de Yel Lissen qui a démontré la persistance de cette protéine Spike plus de 700 jours après les injections anti Covid. Mais il y a aussi une persistance du SARS-CoV 2. Et ceci peut-être en dépit des traitements précoces. J'expliquerai juste après pourquoi. Il y a une persistance de la spi vaccinale, donc comme je viens de vous le décrire, mais également possiblement de l'ARN messager modifié avec une production donc de cette spike des mois après les injections anti covid. Aujourd'hui, a quand même quelques publications assez alarmantes. Dès Crüssfeld Jacob, 14 mois après infection par le SARS-CoV 2. Là, ici, sur ce nouvel, sur cette nouvelle publication des AVC, 17 mois après potentiellement injections plus infections. Et donc je vais vous expliquer pourquoi le SARS-CoV 2 persiste et quelles sont mes dernières recherches. Il faut savoir que la protéine mucocapside du SARS-CoV-2, donc la protéine N du SARS-CoV-2 interagit avec TRIM vingt-huit. C'est quoi TRIM vingt-huit C'est un facteur impliqué dans une grande variété de processus cellulaires comme le matière des cellules souches, la réparation de l'ADN, l'apoptose, l'autophagie, et j'en passe. La perte de Trim 28 lors du développement de l'embryon chez la souris est l'étale. Et Trim 28 peut être impliqué dans de nombreux cancers, globalement. Le problème, c'est que TRIM 28 est aussi impliqué dans l'homéostasie du système immunitaire et dans son activation. Donc, si TRIM 28 est impactée, alors la réponse immunitaire innée en réponse à l'infection par le SARS -CoV 2 est aussi impliquée. Notamment, il va y avoir un délai, un retard dans le lancement de la réponse immunitaire antivirale. Il se peut alors que la réponse immunitaire lors d'une infection par le SARS-CoV 2 soit retardée, et cela va avec les mécanismes de tolérance immunitaire que j'ai précédemment décrits, énormément décrits, notamment avec l'activation du TLR 2 via le système Rage, les cellules myéloïdes, inhibitrices, l'expression de certains HLA inhibiteurs, enfin bref, plus sans compter les propriétés allergènes qui entraînent potentiellement des IgG4. Donc les IgG4 étant un marqueur également de cette de cette tolérance immunitaire. Bref, donc cette interaction de la nucléocapside avec TRIM 28 vient renforcer finalement les actions de la protéine Spike, et donc inhibent complètement la réponse immunitaire innée antivirale, ce qui fait, c'est qu'elle est retardée dans le temps. Qu'est-ce que ça signifie concrètement Il est fort probable qu'il existe une phase, une première phase lors de la contamination virale, qui soit silencieuse, asymptomatique. Puisqu'en fait, les symptômes, ce n'est, ce ne sont que la manifestation d'une activation du système immunitaire. Donc vous comprenez bien que si vous n'avez pas de symptômes, c'est que votre système immunitaire n'est pas activé correctement, et donc votre infection par le SARS-CoV 2 passe dans les premiers temps complètement inaperçue. Autrement dit aussi, nous avons soigné trop tard. Non seulement on n'a soigné que l'hyper inflammation, ne tenant compte que de l'hyper inflammation, sans tenir compte de la tolérance immunitaire, mais également nous avons soigné probablement avec un délai dans le temps. Donc du fait de cette phase asymptomatique, de cette phase retardée. Donc ce qui aurait permis d'ailleurs au virus de s'installer dans l'organisme tranquillou pépère, avant même l'enclenchement des des symptômes, et la mise en place des traitements précoces, dits précoces. Il faut savoir que d'autres virus latent, sont capables d'interagir avec TRIM vingt-huit, pardon. Il y a le b v, le cytomégalovirus, le papillomavirus, l'hépatite b ou encore le vih, le virus responsable du sida. Alors non seulement on a peut-être soigné avec un retard considérable, mais les injections anti Covid ont certainement rajouté une couche supplémentaire, notamment par la surexpression de certains récepteurs qui ont ouvert les portes de l'organisme au virus. En effet, en plus, si la spike virale persiste, le fait de faire produire de la spike par les cellules de l'organisme après l'administration des produits anti Covid, aura probablement eu comme conséquence un effet cumulatif spike viral plus spike vaccinal. De fait, il est rapporté dans la littérature scientifique que les injections, que les infections par le SARS-CoV-2 entraînent des dégâts cumulatifs, et ce, peu importe le statut vaccinal. Je répète, peu importe le statut vaccinal, que vous soyez vacciné ou non vacciné, ça ne change rien. Des infections répétées par le SARS-CoV 2 entraînent des dégâts cumulatifs. Et je pense que nous sommes encore loin du compte en ce qui concerne les dégâts occasionnés par la protéine Spike. Et ce d'autant plus qu'il s'agit d'une arme silencieuse. Elle va, comme je l'ai dit, désactiver le système immunitaire et ça va passer crème. Vous ne sentirez rien jusqu'au point de rupture. Ça veut bien dire qu'on peut déclencher des spycopathies, c'est-à-dire des maladies relatives à la persistance et à la présence de la protéine spike dans l'organisme, qu'elle soit d'origine virale ou vaccinale, dans le temps. Avec un délai, avec un certain retard. L'une des grandes catégories de spycopathies que l'on redoute et qu'on peut redouter énormément, ce sont les atteintes neurologiques. Comme la spike, elle est amyloïde et amyloïdogène. Elle est capable de former en elle-même des fibres hydrogels dégénératives, mais également de faire produire des fibres dégénératives par les cellules de l'organisme, des fibres comme celles qui sont impliquées dans la pathologie d'Alzheimer, de Parkinson, ou même la fibrillation de la protéine prions humaine. Et en plus, on va mettre la cerise sur la tarte au quetch, le virus, grâce à sa spike, peut utiliser ses fibres amyloïdes pour envahir l'organisme potentiellement. Je ne vais pas parler des propriétés allergènes qui peuvent avoir des conséquences comme des syndromes d'activation mastocytaire, Et ça, pas dans le temps, puisqu'elles persistent dans le temps. Donc ça fera comme des mastocytose-like en permanence. Donc comment soigner les spycopathies On a quelques pistes pour soutenir l'organisme, comme la curcumine, l'aspirine. Attention l'aspirine pas pour tout le monde, c'est un inhibiteur de l'activation des plaquettes. Donc si vous êtes sous anticoagulants ou si vous avez d'autres contre indications, ne prenez pas de l'aspirine. La quercétine ou la vitamine D, tout en gardant en tête quand même qu'il ne s'agit que de pansements. Mais c'est mieux que rien. La vitamine D est d'autant plus importante qu'elle peut renforcer la barrière hémato-encéphalique qui est largement attaquée par la protéine spike et le virus. Le fait de retrouver de la spike au niveau des artères cérébrales, ça ne sent pas très bon. Donc cette barrière hématoencéphalique normalement protège notre cerveau et donc elle est un, elle est attaquée, elle est perméabilisée, ce qui ouvre la voie en fait à un virus qui est neurotrope, qui adore le cerveau et qui est ami, avec une protéine Spike qui est amyloïde. Il n'y a pas que la protéine Spike qui est amyloïde, d'accord La protéine N aussi qui est amyloïde. Il y en a d'autres. Mais il nous est aujourd'hui essentiel, en fait, de trouver des outils de diagnostic pour aller chercher, pour aller traquer les spikopathies, notamment des outils de dépistage et de dosage de la protéine Spike, et de développer des thérapies pour bloquer le virus ou éliminer cette protéine Spike, attention, sans enclencher les catastrophes annexes. Il faut aussi traquer le virus, notamment dans les réservoirs, et aller chercher les dégâts tissulaires. On ne soigne pas des dégâts tissulaires comme on soigne une protéine persistante, comme on soigne un virus persistant. Et bien entendu, ces traitements se feront en fonction de votre cas. Chaque individu est différent. Il va donc falloir analyser chez vous ce qui se passe pour aller mieux vous soigner. Voilà. Sur ce, je vous laisse et je vous souhaite une bonne journée, je mettrai les références soit en haut du de la vidéo ou en bas de la vidéo en fonction de comment ça s'agence sur x. Je vous souhaite une bonne journée, au revoir.

@AnneliseBocquet - Bocquet Annelise 🔬🧬📚🚜

Spike, Creutzfeld Jakob et Alzheimer... https://www.news-medical.net/news/20230905/SARS-CoV-2-spike-protein-could-be-speeding-up-Alzheimers-and-other-brain-diseases-says-new-study.aspx Preprint : https://www.biorxiv.org/content/10.1101/2023.09.01.555834v1 Des chercheurs ont évalué les capacités de la protéine Spike du SARS-CoV-2 à induire la fibrillation de la protéine prion PrP ou huPrP (human prion) et des fibres Aβ42. Cette

SARS-CoV-2 spike protein could be speeding up Alzheimer's and other brain diseases, says new study Swedish researchers find that SARS-CoV-2's spike protein amyloids can accelerate the formation of harmful protein aggregates related to neurodegenerative diseases like Creutzfeldt-Jakob and Alzheimer's. The study suggests a potential link between COVID-19 and increased cases of these brain disorders. news-medical.net

SARS-CoV-2 Spike amyloid fibrils specifically and selectively accelerates amyloid fibril formation of human prion protein and the amyloid β peptide bioRxiv - the preprint server for biology, operated by Cold Spring Harbor Laboratory, a research and educational institution biorxiv.org

@AnneliseBocquet - Bocquet Annelise 🔬🧬📚🚜

Thread à lire 🧵! "Le Dr Jordan Vaughn, médecin basé en Alabama, a ensuite fourni une estimation effrayante : jusqu'à 15 millions d'Américains pourraient souffrir de blessures liées à la COVID longue ou au vaccin contre la COVID. Il traite désormais des adolescents qui ne

@AnneliseBocquet - Bocquet Annelise 🔬🧬📚🚜

En parlant d'Alzheimer... Vous saviez que le SARS-CoV-2, le virus qui induit la Covid19, peut promouvoir ou enclencher des pathologies neurodégénératives comme... Alzheimer mais aussi Parkinson ? https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10050697/ https://pubmed.ncbi.nlm.nih.gov/38259635/ https://pubmed.ncbi.nlm.nih.gov/36314211/

The viral hypothesis in Alzheimer’s disease: SARS-CoV-2 on the cusp Increasing evidence highlights that infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has long-term effects on cognitive function, which may cause neurodegenerative diseases like Alzheimer’s disease (AD) in the future. We ... pmc.ncbi.nlm.nih.gov

Unravelling the connection between COVID-19 and Alzheimer's disease: a comprehensive review - PubMed Currently, there exists a limited comprehension regarding the correlation between COVID-19 and Alzheimer's disease (AD). To elucidate the interrelationship and its impact on outcomes, a comprehensive investigation was carried out utilising time-unrestricted searches of reputable databases such as Sc … pubmed.ncbi.nlm.nih.gov

COVID-19 as a Risk Factor for Alzheimer's Disease - PubMed Severe acute respiratory disease coronavirus 2 (SARS-CoV-2) is responsible for the coronavirus disease 2019 (COVID-19) pandemic. Although a primarily respiratory disease, recent reports indicate that it also affects the central nervous system (CNS). Over 25% of COVID-19 patients report neurological … pubmed.ncbi.nlm.nih.gov

@AnneliseBocquet - Bocquet Annelise 🔬🧬📚🚜

Comment vous dire que ça pue, niveau immuno ? Les injections anti-covid perdent de leur efficacité au niveau des lymphocytes T? Sans blague... impact d'une exposition répétée à un même antigène ! https://onlinelibrary.wiley.com/doi/10.1002/jmv.29790?af=R La 3e dose (3D) a augmenté le pourcentage de résidents

@AnneliseBocquet - Bocquet Annelise 🔬🧬📚🚜

Hé... 2025 : PVS - épuisement des lymphocytes, hein... rien que ça ! Comme quoi...

@AnneliseBocquet - Bocquet Annelise 🔬🧬📚🚜

2/2 3. Similitudes entre PVS et Covid-long : a. Les symptômes cliniques : Les deux conditions partagent des phénotypes cliniques similaires, comme la fatigue chronique, la dysautonomie, et les troubles cognitifs, souvent attribués à l’épuisement immunitaire. b. L'épuisement

@AnneliseBocquet - Bocquet Annelise 🔬🧬📚🚜

Coenzyme Q10 pour soigner les covid-longs ? https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10779395/ Les mitochondries jouent un rôle important dans la réponse aux infections virales. Elles sont, en effet, impliquées dans la production de radicaux oxygénés et de l'initiation de la réponse immunitaire via les

Mitochondrial Dysfunction and Coenzyme Q10 Supplementation in Post-Viral Fatigue Syndrome: An Overview Post-viral fatigue syndrome (PVFS) encompasses a wide range of complex neuroimmune disorders of unknown causes characterised by disabling post-exertional fatigue, myalgia and joint pain, cognitive impairments, unrefreshing sleep, autonomic ... pmc.ncbi.nlm.nih.gov

@AnneliseBocquet - Bocquet Annelise 🔬🧬📚🚜

Dans la série des "bonnes nouvelles" : la Spike du SARS-CoV-2 est génotoxique... semble-t-il. - Par des mécanismes indirects comme le stress oxydatif ou son impact sur les mitochondries... - Par des mécanismes directs en interférant avec des mécanismes de réparations et de

@AnneliseBocquet - Bocquet Annelise 🔬🧬📚🚜

Spike, p53 et mitochondries... Allez, je vais essayer de vulgariser. 1. Interaction Spike/p53 et immunité : La Spike pourrait interagir avec p53, qui est un régulateur clé de l’immunité innée et adaptative, notamment via la production d’interférons (IFN) de type I et de gènes

@AnneliseBocquet - Bocquet Annelise 🔬🧬📚🚜

"Preuves du potentiel bacteriophage du SARS-CoV-2 dans le microbiote intestinal humain" Petrillo et al., 23 avril 2025. https://pubmed.ncbi.nlm.nih.gov/40444030/ Le virus responsable de la COVID-19, le SARS-CoV-2, fut détecté dans des cultures de bactéries, à l'extérieur et à l'intérieur des

Evidence of SARS-CoV-2 bacteriophage potential in human gut microbiota - PubMed Based on these results we conclude that, in addition to its well-documented interactions with eukaryotic cells, SARS-CoV-2 may act as a bacteriophage when interacting with at least two bacterial species known to be present in the human microbiota. If the hypothesis proposed, i.e., that under certain … pubmed.ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

It was three years ago that I was sitting at my desk when I received a phone call from a client who believed there was an issue with my software as he was unable to locate information on a spreadsheet. It was there but he was suffering from "brain fog."

@dbdugger - Daniel Brittain Dugger

This article, published the same year, was among the first returned in the search results. Cerebrospinal Fluid Offers Clues to Post-COVID ‘Brain Fog’ https://www.ucsf.edu/news/2022/01/422156/cerebrospinal-fluid-offers-clues-post-covid-brain-fog

@dbdugger - Daniel Brittain Dugger

"All participants underwent an in-person cognitive testing battery with a neuropsychologist, applying equivalent criteria used for HIV-associated neurocognitive disorder (HAND)."

@dbdugger - Daniel Brittain Dugger

"Surprisingly, the researchers found that 13 of the 22 participants (59 percent) with cognitive symptoms met HAND criteria, compared with seven of the 10 control participants (70 percent)."

@dbdugger - Daniel Brittain Dugger

Observing cognitive impairment equal in magnitude to that of HIV Associated Neurocognitive Decline confirms the hypothesis advanced by Kenneth Podell on September 29th, 2020. Multiple Neuroinvasive Pathways in COVID-19 https://pubmed.ncbi.nlm.nih.gov/32990925/

Multiple Neuroinvasive Pathways in COVID-19 - PubMed COVID-19 is a highly infectious viral disease caused by the novel coronavirus SARS-CoV-2. While it was initially regarded as a strictly respiratory illness, the impact of COVID-19 on multiple organs is increasingly recognized. The brain is among the targets of COVID-19, and it can be impacted in mul … pubmed.ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

"One can draw on the experience with an HIV/AIDS epidemic. The initial understanding of HIV/AIDS was that of the virus affecting the immune system by depleting T cells, which resulted in opportunistic infections of multiple organs, including the brain."

@dbdugger - Daniel Brittain Dugger

"However, it did not take long to discover that the disease could also attack the brain directly, which resulted in long-term cognitive impairment."

@dbdugger - Daniel Brittain Dugger

"Subsequently, HIV encephalopathy and AIDS dementia complex leading to long-term cognitive impairment were discovered [87]. Based on the emerging literature, it is reasonable to hypothesize a somewhat similar scenario may unfold in relationship to COVID-19."

@dbdugger - Daniel Brittain Dugger

The equivalent criteria is that of the Frascati Criteria which recognizes Asymptomatic Neurocognitive Impairment, Mild Neurocognitive Decline, and AIDS Dementia Complex.

@dbdugger - Daniel Brittain Dugger

HIV-associated neurocognitive disorder — pathogenesis and prospects for treatment https://pmc.ncbi.nlm.nih.gov/articles/PMC4937456/

HIV-associated neurocognitive disorder — pathogenesis and prospects for treatment In the past two decades, several advancements have improved the care of HIV-infected individuals. Most importantly, the development and deployment of combination antiretroviral therapy (CART) has resulted in a dramatic decline in the rate of deaths ... pmc.ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

Asymptomatic neurocognitive impairment (ANI) Impairment in ≥2 neurocognitive domains (≥1 SD) Does not interfere with daily functioning

@dbdugger - Daniel Brittain Dugger

Mild neurocognitive disorder (MND) Impairment in ≥2 neurocognitive domains (≥1 SD) Mild to moderate interference in daily functioning

@dbdugger - Daniel Brittain Dugger

HIV-associated dementia (HAD) Marked (≥2 SD) impairment in ≥2 neurocognitive domains Marked interference in daily functioning

@dbdugger - Daniel Brittain Dugger

Those now diagnosed with ME/CFS were among those living with ANI at a two-to-six times increase risk of conversion and did so in a way we have observed over the past forty years.

@dbdugger - Daniel Brittain Dugger

"Despite being asymptomatic, ANI is clinically relevant because individuals with ANI can transition to one of the more severe forms of HAND:"

@dbdugger - Daniel Brittain Dugger

"for example, participants of the CNS HIV Antiretroviral Therapy Effects Research (CHARTER) study who had ANI at baseline were two to six times more likely to develop symptomatic HAND during several years of follow-up than those who were neurocognitively normal at baseline."

@dbdugger - Daniel Brittain Dugger

Could You Have ME/CFS? (Myalgic Encephalomyelitis/Chronic Fatigue Syndrome) https://www.cdc.gov/me-cfs/pdfs/could-you-have-mecfs_508.pdf ME/CFS is a complex illness and symptoms of ME/CFS may seem similar to many other illnesses. ME/CFS requires three symptoms:

@dbdugger - Daniel Brittain Dugger

See? They are unable to complete their ADLs. 1. Not being able to participate in routine activities that were possible before becoming ill, such as work, school, social life, and/or personal life, that:

@dbdugger - Daniel Brittain Dugger

• Lasts for more than 6 months • Is accompanied by fatigue that is: • Often serious • Just started (not lifelong) • Not the result of ongoing activities • Not from more than usual effort • Not made better by rest

@dbdugger - Daniel Brittain Dugger

It was in December of 2021 that Dr. Daniel Chertow implicated the two most well known reservoirs in HIV, that of the Central Nervous System and Gut Associated Lymphoid Tissues.

@dbdugger - Daniel Brittain Dugger

SARS-CoV-2 infection and persistence throughout the human body and brain December 2021 https://www.researchgate.net/publication/357197928_SARS-CoV-2_infection_and_persistence_throughout_the_human_body_and_brain

@dbdugger - Daniel Brittain Dugger

The very same month, China published this paper demonstrating the efficacy of Azvudine. Published: 06 December 2021 Azvudine is a thymus-homing anti-SARS-CoV-2 drug effective in treating COVID-19 patients https://www.nature.com/articles/s41392-021-00835-6

Azvudine is a thymus-homing anti-SARS-CoV-2 drug effective in treating COVID-19 patients - Signal Transduction and Targeted Therapy Azvudine (FNC) is a nucleoside analog that inhibits HIV-1 RNA-dependent RNA polymerase (RdRp). Recently, we discovered FNC an agent against SARS-CoV-2, and have taken it into Phase III trial for COVID-19 patients. FNC monophosphate analog inhibited SARS-CoV-2 and HCoV-OC43 coronavirus with an EC50 between 1.2 and 4.3 μM, depending on viruses or cells, and selective index (SI) in 15–83 range. Oral administration of FNC in rats revealed a substantial thymus-homing feature, with FNC triphosphate (the active form) concentrated in the thymus and peripheral blood mononuclear cells (PBMC). Treating SARS-CoV-2 infected rhesus macaques with FNC (0.07 mg/kg, qd, orally) reduced viral load, recuperated the thymus, improved lymphocyte profiles, alleviated inflammation and organ damage, and lessened ground-glass opacities in chest X-ray. Single-cell sequencing suggested the promotion of thymus function by FNC. A randomized, single-arm clinical trial of FNC on compassionate use (n = 31) showed that oral FNC (5 mg, qd) cured all COVID-19 patients, with 100% viral ribonucleic acid negative conversion in 3.29 ± 2.22 days (range: 1–9 days) and 100% hospital discharge rate in 9.00 ± 4.93 days (range: 2–25 days). The side-effect of FNC is minor and transient dizziness and nausea in 16.12% (5/31) patients. Thus, FNC might cure COVID-19 through its anti-SARS-CoV-2 activity concentrated in the thymus, followed by promoted immunity. nature.com

@dbdugger - Daniel Brittain Dugger

It is through the protein it specifically targets that explains the use of cats to study Long Covid. What Cats May Teach Us About Long COVID https://www.ucdavis.edu/health/news/what-cats-may-teach-us-about-long-covid

What Cats May Teach Us About Long COVID UC Davis researchers find cats could help us learn about long COVID. They've found a new cell therapy boosts immune systems in cats with severe coronavirus. ucdavis.edu

@dbdugger - Daniel Brittain Dugger

"Feline infectious peritonitis, or FIP, is a serious and historically fatal disease in cats caused by a coronavirus. It behaves in many ways like severe coronavirus infections in humans, causing widespread inflammation, T cell exhaustion and chronic immune dysfunction."

@dbdugger - Daniel Brittain Dugger

The first Chinese oral anti-COVID-19 drug Azvudine launched https://pmc.ncbi.nlm.nih.gov/articles/PMC9461232/

The first Chinese oral anti-COVID-19 drug Azvudine launched pmc.ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

"Particularly, Azvudine (FNC, 2′-deoxy-2′-β-fluoro-4′-azidocytidine) targets reverse transcriptase and HIV-1 accessory protein (Vif) simultaneously, being the first-in-class dual inhibitor."

@dbdugger - Daniel Brittain Dugger

See? It all falls into place like cats fall into laps. Determinants of FIV and HIV Vif sensitivity of feline APOBEC3 restriction factors https://pubmed.ncbi.nlm.nih.gov/27368163/

Determinants of FIV and HIV Vif sensitivity of feline APOBEC3 restriction factors - PubMed Here we identified in feline A3s residues important for binding of FIV Vif and a unique protein domain insertion (linker). To understand Vif evolution, a structural model of the feline A3 was developed. Our results show that HIV Vif binds human A3s differently than FIV Vif feline A3s. The linker ins … pubmed.ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

Our failure to engage in a similar antiviral strategy has left the Central Nervous System reservoir of millions to expand in the same way observed in the HIV+ and each cell type that constitutes that reservoir to be productively infected for years.

@dbdugger - Daniel Brittain Dugger

Nef-like mediated damage has been observed for several years, with 2022, 2023, 2024, and 2025 being relevant to cognitive impairment.

@dbdugger - Daniel Brittain Dugger

It was in 2022 that we learned Tunneling Nanotubes are expanding the Central Nervous System reservoir of millions. Tunneling nanotubes provide a route for SARS-CoV-2 spreading https://pubmed.ncbi.nlm.nih.gov/35857849/

Tunneling nanotubes provide a route for SARS-CoV-2 spreading - PubMed Neurological manifestations of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection represent a major issue in long coronavirus disease. How SARS-CoV-2 gains access to the brain and how infection leads to neurological symptoms are not clear because the principal means of viral entr … pubmed.ncbi.nlm.nih.gov

@dbdugger — Daniel Brittain Dugger

Posted - June 28, 2025 at 10:34 AM

Saved - June 28, 2025 at 12:17 PM

reSee.it AI Summary

I noted that Harry blocked me after I drew parallels between HIV and Long Covid, focusing on immune and cognitive impacts. I discussed the role of Protein E, akin to HIV's Tat, and its implications for neurodegeneration. Evidence suggests that the neurovascular unit in Long Covid patients is damaged similarly to HIV. I highlighted studies connecting cytokine responses, monocyte behavior, and amyloid deposition in both conditions. The evolving understanding of these mechanisms raises concerns about cognitive impairment and the need for further research.

@dbdugger - Daniel Brittain Dugger

Harry took the liberty of blocking me after as I have drawn parallels to HIV after reading and in an attempt to preserve the autonomy, immune competence, and cognition. The HIV- once again decided to betray the HIV+. That which appears below? Has been studied for fourteen years.

@DavidJoffe64 - David Joffe MB BS (Hons), PhD, FRACP 🇦🇺

🧠 Daily Feed of Brain Damage 🧠 @HarrySpoelstra ☠️☠️

@HarrySpoelstra - Harry Spoelstra

Immunomodulatory Mechanisms Underlying Neurological Manifestations in Long COVID: Implications for Immune-Mediated Neurodegeneration 🔥Your homework for this weekend!😷 ‼️Neuroimmune dysfunction/Braindamage following SARS-CoV-2 infection ➡️This very interesting narrative

@dbdugger - Daniel Brittain Dugger

What is quite ironic about Protein E, operating mechanistically as HIV's Tat, is that it contributes to that which you will not observe in those living with ME/CFS.

@dbdugger - Daniel Brittain Dugger

This article clearly makes the connection between Protein E and HIV's Tat and will be relevant as the thread develops. SARS-CoV-2 Viroporin E Induces Ca2+ Release and Neuron Cell Death in Primary Cultures of Rat Hippocampal Cells Aged In Vitro https://pmc.ncbi.nlm.nih.gov/articles/PMC11203731/

SARS-CoV-2 Viroporin E Induces Ca2+ Release and Neuron Cell Death in Primary Cultures of Rat Hippocampal Cells Aged In Vitro The COVID-19 pandemic was caused by infection with Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), which may lead to serious respiratory, vascular and neurological dysfunctions. The SARS-CoV-2 envelope protein (E protein) is a ... pmc.ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

"Highly infectious viruses such as the human immunodeficiency virus (HIV), Ebola virus, or hepatitis C virus encode proteins that function as ion channels."

@dbdugger - Daniel Brittain Dugger

SARS-CoV-2 targets ribosomal RNA biogenesis https://www.cell.com/cell-reports/pdf/S2211-1247(24)00219-5.pdf

@dbdugger - Daniel Brittain Dugger

"Finally, the Tat protein of human immunodeficiency virus interacts with FBL and U3 snoRNA, impairing prerRNA processing and depleting mature ribosomes."

@dbdugger - Daniel Brittain Dugger

Same Tat. Same hippocampus. Same Ca2+ overload. HIV-1 protein Tat induces apoptosis of hippocampal neurons by a mechanism involving caspase activation, calcium overload, and oxidative stress https://pubmed.ncbi.nlm.nih.gov/9878167/

HIV-1 protein Tat induces apoptosis of hippocampal neurons by a mechanism involving caspase activation, calcium overload, and oxidative stress - PubMed Patients infected with HIV-1 often exhibit cognitive deficits that are related to progressive neuronal degeneration and cell death. The protein Tat, which is released from HIV-1-infected cells, was recently shown to be toxic toward cultured neurons. We now report that Tat induces apoptosis in cultur … pubmed.ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

Having read volumes, there is little question but that the neurovascular unit of those living with Long Covid is being destroyed in the very exact same way observed in the HIV.

@dbdugger - Daniel Brittain Dugger

Astrocytes, HIV and the Glymphatic System: A Disease of Disrupted Waste Management? https://pmc.ncbi.nlm.nih.gov/articles/PMC7550659/

Astrocytes, HIV and the Glymphatic System: A Disease of Disrupted Waste Management? The discovery of the glial-lymphatic or glymphatic fluid clearance pathway in the rodent brain led researchers to search for a parallel system in humans and to question the implications of this pathway in neurodegenerative diseases. Magnetic ... pmc.ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

The graphic in the quoted tweet references Blood Brain Barrier degradation and immune system infiltration. We have only known of both since October of 2021.

@dbdugger - Daniel Brittain Dugger

The productive infection of brain pericytes was reported in October of 2021. 2021 Oct 27 Infection of Brain Pericytes Underlying Neuropathology of COVID-19 Patients https://pubmed.ncbi.nlm.nih.gov/34769052/

Infection of Brain Pericytes Underlying Neuropathology of COVID-19 Patients - PubMed A wide range of neurological manifestations have been associated with the development of COVID-19 following SARS-CoV-2 infection. However, the etiology of the neurological symptomatology is still largely unexplored. Here, we used state-of-the-art multiplexed immunostaining of human brains (n … pubmed.ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

Their dysregulation is known to contribute to Blood Brain Barrier degradation and Cerebral Blood Flow disturbances. This article addresses the role of Platelet Derived Growth Factor-BB in the context of a SARS-Cov-2 infection.

@dbdugger - Daniel Brittain Dugger

SARS-CoV-2 infection- induced growth factors play differential roles in COVID-19 pathogenesis https://pmc.ncbi.nlm.nih.gov/articles/PMC9188443/

SARS-CoV-2 infection- induced growth factors play differential roles in COVID-19 pathogenesis Biologically active molecules cytokines and growth factors (GFs) are critical regulators of tissue injury/repair and emerge as key players in COVID-19 pathophysiology. However, specific disease stage of GFs dysregulation and, whether these GFs have ... pmc.ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

In the HIV+, it is Tat that contributes to a loss of brain pericyte coverage at the Blood Brain Barrier through a reliance upon the very thing mentioned above, PDGF-BB. HIV Tat 101-mediated loss of pericytes at the blood-brain barrier involves PDGF-BB https://pmc.ncbi.nlm.nih.gov/articles/PMC4444060/

HIV Tat 101-mediated loss of pericytes at the blood-brain barrier involves PDGF-BB HIV-1-associated neurocognitive disorders (HAND) affect almost 30-50% of infected individuals, even in the presence of successful control of virus replication by combined antiretroviral therapy (cART).HIV Tat protein, a nuclear trans-activator of ... pmc.ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

There are those who still support Ivermectin. Are they planning trying to deworm Trojan Horses? 2021 Oct 28 Macrophages and Monocytes: “Trojan Horses” in COVID-19 https://pmc.ncbi.nlm.nih.gov/articles/PMC8624282/

Macrophages and Monocytes: “Trojan Horses” in COVID-19 We aimed to explore whether variants of SARS-CoV-2 (Chinese-derived strain (D614, lineage A), Italian strain PV10734 (D614G, lineage B.1.1) and Alpha strain (lineage B.1.1.7)) were able to infect monocytes (MN) and monocyte-derived macrophages (MDM) ... pmc.ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

The Hypothesis, long recognized in HIV. Monocytes cross a compromised BBB and if programmed to do so, differentiate into the primary target of HIV within the CNS, perivascular macrophages.

@dbdugger - Daniel Brittain Dugger

Those in academia, the medical establishment, and "advocacy" groups find themselves with the legacy of having destroyed the cognition of their income source after first ignoring and then allow for conversion from Asymptomatic Neurocognitive Impairment.

@dbdugger - Daniel Brittain Dugger

That their income source is suffering from ANI, not observed in ME/CFS, has only been known since January of 2022. January 18, 2022 Cerebrospinal Fluid Offers Clues to Post-COVID ‘Brain Fog’ https://www.ucsf.edu/news/2022/01/422156/cerebrospinal-fluid-offers-clues-post-covid-brain-fog

@dbdugger - Daniel Brittain Dugger

"All participants underwent an in-person cognitive testing battery with a neuropsychologist, applying equivalent criteria used for HIV-associated neurocognitive disorder (HAND)."

@dbdugger - Daniel Brittain Dugger

"Surprisingly, the researchers found that 13 of the 22 participants (59 percent) with cognitive symptoms met HAND criteria, compared with seven of the 10 control participants (70 percent)."

@dbdugger - Daniel Brittain Dugger

If the reliance upon the Frascati Criteria to stage the cognitive impairment of those living with Long Covid rings a bell, it was suggested prudent to do by Kenneth Podell on September 29th, 2020.

@dbdugger - Daniel Brittain Dugger

Epub 2020 Sep 29. Multiple Neuroinvasive Pathways in COVID-19 https://pubmed.ncbi.nlm.nih.gov/32990925/

@dbdugger - Daniel Brittain Dugger

"However, it did not take long to discover that the disease could also attack the brain directly, which resulted in long-term cognitive impairment."

@dbdugger - Daniel Brittain Dugger

That which contributed to the profoundness of the ANI observed in the control arm? Elevated monocytes, ready to differentiate into perivascular macrophages, whose relatively quick turnover is responsible for the appearance and disappearance of virus in the CNS reservoir.

@dbdugger - Daniel Brittain Dugger

Monocytosis in the acute phase of SARS-CoV-2 infection predicts the presence of anosognosia for cognitive deficits in the chronic phase https://pmc.ncbi.nlm.nih.gov/articles/PMC9477785/

Monocytosis in the acute phase of SARS-CoV-2 infection predicts the presence of anosognosia for cognitive deficits in the chronic phase Reduced awareness of neuropsychological disorders (i.e., anosognosia) is a striking symptom of post-COVID-19 condition. Some leukocyte markers in the acute phase may predict the presence of anosognosia in the chronic phase, but they have not yet ... pmc.ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

It was in 2022 that we learned of the productive infection of astrocytes, well known reservoirs in HIV, as evidenced by this title. 2022 Jul 18 In SARS-CoV-2, astrocytes are in it for the long haul https://pmc.ncbi.nlm.nih.gov/articles/PMC9335203/

In SARS-CoV-2, astrocytes are in it for the long haul pmc.ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

It was in November of that same year three hypotheses were advanced to explain amyloid deposition. 2022 Nov 11 SARS-CoV-2-Induced Amyloidgenesis: Not One, but Three Hypotheses for Cerebral COVID-19 Outcomes https://pmc.ncbi.nlm.nih.gov/articles/PMC9692683/

SARS-CoV-2-Induced Amyloidgenesis: Not One, but Three Hypotheses for Cerebral COVID-19 Outcomes The main neuropathological feature of Alzheimer’s disease (AD) is extracellular amyloid deposition in senile plaques, resulting from an imbalance between the production and clearance of amyloid beta peptides. Amyloid deposition is also found around ... pmc.ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

The graphic from the quoted tweet mentions cerebral microbleeds. The article above addresses Cerebral Amyloid Angiopathy. "Amyloid deposition is also found around cerebral blood vessels, termed cerebral amyloid angiopathy (CAA), in 90% of AD cases."

@dbdugger - Daniel Brittain Dugger

The graphic from the paper Harry shared addresses endothelial dysfunction. The article above addresses the same.

@dbdugger - Daniel Brittain Dugger

"We highlight the role of astrocytes and endothelial cells in the process of amyloidgenesis, as well as the role of other amyloidgenic proteins, such as fibrinogen and serum amyloid A protein, in addition to the neuronal amyloid precursor protein."

@dbdugger - Daniel Brittain Dugger

This paper addresses the productive infection of brain microvascular cells through involvement of the same pathway they mentioned, NF-kB.

@dbdugger - Daniel Brittain Dugger

SARS-CoV-2 infection of human brain microvascular endothelial cells leads to inflammatory activation through NF-κB non-canonical pathway and mitochondrial remodeling https://pmc.ncbi.nlm.nih.gov/articles/PMC9216729/

SARS-CoV-2 infection of human brain microvascular endothelial cells leads to inflammatory activation through NF-κB non-canonical pathway and mitochondrial remodeling Neurological effects of COVID-19 and long-COVID-19 as well as neuroinvasion by SARS-CoV-2 still pose several questions and are of both clinical and scientific relevance. We described the cellular and molecular effects of the human brain ... pmc.ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

The authors in the paper Harry shared mentioned that which has been known since December of 2020, Tight Junction destruction. 2020 Dec 23 SARS-CoV-2 Envelope (E) Protein Interacts with PDZ-Domain-2 of Host Tight Junction Protein ZO1 https://pmc.ncbi.nlm.nih.gov/articles/PMC7781303/

SARS-CoV-2 Envelope (E) Protein Interacts with PDZ-Domain-2 of Host Tight Junction Protein ZO1 Newly emerged SARS-CoV-2 is the cause of an ongoing global pandemic leading to severe respiratory disease in humans. SARS-CoV-2 targets epithelial cells in the respiratory tract and lungs, which can lead to amplified chloride secretion and increased ... pmc.ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

Same Tat. Same brain microvascular endothelial cells. Same Tight Junction destruction. Disruption of blood–brain barrier: effects of HIV Tat on brain microvascular endothelial cells and tight junction proteins https://link.springer.com/article/10.1007/s13365-023-01179-3

Disruption of blood–brain barrier: effects of HIV Tat on brain microvascular endothelial cells and tight junction proteins - Journal of NeuroVirology Although the widespread use of antiretroviral therapy (ART) has prolonged the life span of people living with HIV (PLWH), the incidence of HIV-associated n link.springer.com

@dbdugger - Daniel Brittain Dugger

The three hypotheses advanced were "Several receptors for SAA have been identified, including scavenger-receptor SR-B1 (involved in cholesterol efflux and removal of SAA), toll-like receptors 2 (TLR2) and 4 (TLR4), and receptor for advanced glycated end-products (RAGE)....."

@dbdugger - Daniel Brittain Dugger

The authors of the paper shared above mentions astrocyte activation, for which GFAP is used as a biomarker. Among the articles describing its elevation. A Prospective Study on Neural Biomarkers in Patients with Long-COVID Symptoms https://pmc.ncbi.nlm.nih.gov/articles/PMC10971257/

A Prospective Study on Neural Biomarkers in Patients with Long-COVID Symptoms Background: this prospective observational study aims to assess serum levels of glial fibrillary acidic protein (GFAP), s100b, and total Tau in long-COVID patients, exploring correlations with symptoms, cognitive decline, mental health, and quality ... pmc.ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

In the HIV+, it is Tat that leads to its elevation in the brain and bowel.

@dbdugger - Daniel Brittain Dugger

HIV-1 Tat Induces Unfolded Protein Response and Endoplasmic Reticulum Stress in Astrocytes and Causes Neurotoxicity through Glial Fibrillary Acidic Protein (GFAP) Activation and Aggregation HIV-1 Tat is a major culprit for HIV/neuroAIDS. One of the consistent hallmarks of HIV/neuroAIDS is reactive astrocytes or astrocytosis, characterized by increased cytoplasmic accumulation of the intermediate filament glial fibrillary acidic protein ... pmc.ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

The paper shared by Harry mentions IL-6, TNF-a, and S100b but fails to mention another cytokine that is elevated in the SARS-Cov-2 and HIV+, IL-1b.

@dbdugger - Daniel Brittain Dugger

We have known individuals are becoming cachexic, or suffering from wasting syndrome defined as diarrhea lasting for thirty days with a concomitant ten % reduction in total body weight for ten years.

@dbdugger - Daniel Brittain Dugger

2020 Jun 9 COVID‐19: a major cause of cachexia and sarcopenia? https://pmc.ncbi.nlm.nih.gov/articles/PMC7300782/

COVID‐19: a major cause of cachexia and sarcopenia? pmc.ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

In the HIV+, Tat contributes to intractable diarrhea and through stimulation of the enteric nervous system, allows for secretion of S100b, IL-6, TNF-a, and IL-1b.

@dbdugger - Daniel Brittain Dugger

HIV-1 Tat-induced diarrhea evokes an enteric glia-dependent neuroinflammatory response in the central nervous system https://www.nature.com/articles/s41598-017-05245-9

HIV-1 Tat-induced diarrhea evokes an enteric glia-dependent neuroinflammatory response in the central nervous system - Scientific Reports Despite the effectiveness of combined anti-retroviral therapy, human immunodeficiency virus (HIV) infected-patients frequently report diarrhea and neuropsychological deficits. It is claimed that the viral HIV-1 Trans activating factor (HIV-1 Tat) protein is responsible for both diarrhea and neurotoxic effects, but the underlying mechanisms are not known. We hypothesize that colonic application of HIV-1 Tat activates glial cells of the enteric nervous system (EGCs), leading to a neuroinflammatory response able to propagate to the central nervous system. We demonstrated that HIV-1 Tat-induced diarrhea was associated with a significant activation of glial cells within the colonic wall, the spinal cord and the frontal cortex, and caused a consistent impairment of the cognitive performances. The inhibition of glial cells activity by lidocaine, completely abolished the above-described effects. These observations point out the role of glial cells as putative effectors in HIV-1 Tat-associated gastrointestinal and neurological manifestations and key regulators of gut-brain signaling. nature.com

@dbdugger - Daniel Brittain Dugger

The IL-1β, IL-6, and TNF cytokine triad is associated with post-acute sequelae of COVID-19 https://www.sciencedirect.com/science/article/pii/S2666379122001951

The IL-1β, IL-6, and TNF cytokine triad is associated with post-acute sequelae of COVID-19 Post-acute sequelae of COVID-19 (PASC) is emerging as global problem with unknown molecular drivers. Using a digital epidemiology approach, we recruit… sciencedirect.com

@dbdugger - Daniel Brittain Dugger

In the HIV+, it is Tat that leads to the upregulation of RAGE receptors within the perivascular end-feet of astrocytes found within the Blood Brain Barrier with resultant amyloid deposition.

@dbdugger - Daniel Brittain Dugger

HIV-1 Tat Upregulates the Receptor for Advanced Glycation End Products and Superoxide Dismutase-2 in the Heart of Transgenic Mice https://www.mdpi.com/1999-4915/14/10/2191

@dbdugger - Daniel Brittain Dugger

"Recent studies have indicated that HIV-1 Tat-induced RAGE expression within the blood–brain barrier accelerates amyloid beta deposition."

@dbdugger - Daniel Brittain Dugger

In the HIV+, Tat, when found within astrocytes at the BBB, leads to elevated MCP, which calls the Trojan Horses into the CNS reservoir.

@dbdugger - Daniel Brittain Dugger

HIV-1 Tat induces monocyte chemoattractant protein-1-mediated monocyte transmigration across a model of the human blood-brain barrier and up-regulates CCR5 expression on human monocytes - PubMed AIDS dementia is characterized by neuronal loss in association with synaptic damage. A central predictor for clinical onset of these symptoms is the infiltration of monocytes and macrophages into CNS parenchyma. Chronic HIV-1 infection of monocytes also allows these cells to serve as reservoirs for … pubmed.ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

While we have long known of a protein operating mechanistically as HIV's Nef, it was in 2023 that Akiko Iwasaki proved she was willing to betray millions and cholesterol efflux pathway involvement was made known.

@dbdugger - Daniel Brittain Dugger

Akiko Iwasaki Enhanced inhibition of MHC-I expression by SARS-CoV-2 Omicron subvariants https://pmc.ncbi.nlm.nih.gov/articles/PMC10120007/

Enhanced inhibition of MHC-I expression by SARS-CoV-2 Omicron subvariants Numerous pathogenic viruses have developed strategies to evade host CD8+ T cell-mediated clearance. Here, we demonstrated that SARS-CoV-2 encodes multiple viral factors that can modulate major histocompatibility complex class I (MHC-I) expression in ... pmc.ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

"We also included HIV Nef as a positive control for downregulating both MHC-I and MHC-II (30, 31), and SARS-CoV ORF8a/b proteins as a negative control."

@dbdugger - Daniel Brittain Dugger

She also observed Protein E once again operating mechanistically as HIV's Tat. "We found that in addition to ORF8, SARS-CoV-2 E, M, and ORF7a substantially down-regulated MHC-I within the cells expressing these viral proteins."

@dbdugger - Daniel Brittain Dugger

Repression of MHC Class I Gene Promoter Activity by Two-Exon Tat of HIV https://www.science.org/doi/10.1126/science.8493575

@dbdugger - Daniel Brittain Dugger

September of that same year, evidence of foam cell formation emerged and that it is occurring can be explained by cholesterol efflux pathway impairment.

@dbdugger - Daniel Brittain Dugger

Published: 28 September 2023 SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary vessels https://www.nature.com/articles/s44161-023-00336-5

SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary vessels - Nature Cardiovascular Research Patients with coronavirus disease 2019 (COVID-19) present increased risk for ischemic cardiovascular complications up to 1 year after infection. Although the systemic inflammatory response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection likely contributes to this increased cardiovascular risk, whether SARS-CoV-2 directly infects the coronary vasculature and attendant atherosclerotic plaques remains unknown. Here we report that SARS-CoV-2 viral RNA is detectable and replicates in coronary lesions taken at autopsy from severe COVID-19 cases. SARS-CoV-2 targeted plaque macrophages and exhibited a stronger tropism for arterial lesions than adjacent perivascular fat, correlating with macrophage infiltration levels. SARS-CoV-2 entry was increased in cholesterol-loaded primary macrophages and dependent, in part, on neuropilin-1. SARS-CoV-2 induced a robust inflammatory response in cultured macrophages and human atherosclerotic vascular explants with secretion of cytokines known to trigger cardiovascular events. Our data establish that SARS-CoV-2 infects coronary vessels, inducing plaque inflammation that could trigger acute cardiovascular complications and increase the long-term cardiovascular risk. Eberhardt et al. show that SARS-CoV-2 infects human coronary lesions where it preferentially targets plaque macrophages, triggering plaque inflammation and potentially leading to acute cardiovascular complications and long-term cardiovascular risks in patients with COVID-19. nature.com

@dbdugger - Daniel Brittain Dugger

"33. Collins, K. L., Chen, B. K., Kalams, S. A., Walker, B. D. & Baltimore, D. HIV-1 Nef protein protects infected primary cells against killing by cytotoxic T lymphocytes. Nature 391, 397–401 (1998)."

@dbdugger - Daniel Brittain Dugger

It is through proposed therapeutics for those living with Long Covid that evidence is provided of a protein operating mechanistically as HIV's Nef being found within astrocytes.

@dbdugger - Daniel Brittain Dugger

2024 Jul 29. SARS-CoV-2 spike protein acts as a β-adrenergic receptor agonist: A potential mechanism for cardiac sequelae of long COVID https://pubmed.ncbi.nlm.nih.gov/39073192/

SARS-CoV-2 spike protein acts as a β-adrenergic receptor agonist: A potential mechanism for cardiac sequelae of long COVID - PubMed Severe acute respiratory syndrome-coronavirus-2 spike proteins act as an allosteric β-AR agonist, leading to cardiac β-AR hyperactivity, thus contributing to PASC-CVS. pubmed.ncbi.nlm.nih.gov

@dbdugger — Daniel Brittain Dugger

Posted - June 17, 2025 at 11:42 PM

Saved - June 18, 2025 at 10:23 AM

reSee.it AI Summary

I express concern over the cardiovascular complications, particularly Corrected QT Interval Prolongation, that children are facing, which seems overlooked by many. I reference the harmful impact of the Tat protein from HIV on ribosomal RNA biogenesis and its connection to cardiovascular diseases. I highlight the frequent occurrence of QTc prolongation in HIV-positive patients, emphasizing its predictive nature for cardiovascular mortality. I challenge those who downplay the similarities between COVID-19 and HIV, warning of the potential consequences of such dismissals.

@dbdugger - Daniel Brittain Dugger

Agenda? Children have been left to suffer Tat-like cardiovascular complications, including Corrected QT Interval Prolongation. Too bad you don't know what you are talking about.

@thereal_truther - The Real Truther

Shame on all of you exploiting a tragedy for your own agenda.

@dbdugger - Daniel Brittain Dugger

SARS-CoV-2 targets ribosomal RNA biogenesis https://www.cell.com/cell-reports/pdf/S2211-1247(24)00219-5.pdf "Finally, the Tat protein of human immunodeficiency virus interacts with FBL and U3 snoRNA, impairing prerRNA processing and depleting mature ribosomes."

@dbdugger - Daniel Brittain Dugger

COVID-19 Infection and Corrected QT Interval Prolongation—Collateral Damage From Our Newest Enemy https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2779057

@dbdugger - Daniel Brittain Dugger

The role of HIV Tat protein in HIV-related cardiovascular diseases https://pmc.ncbi.nlm.nih.gov/articles/PMC5941636/

The role of HIV Tat protein in HIV-related cardiovascular diseases The human immunodeficiency virus (HIV) is a major global public health issue. HIV-related cardiovascular disease remains a leading cause of morbidity and mortality in HIV positive patients. HIV Tat is a regulatory protein encoded by tat gene of ... pmc.ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

Same Tat. Same Corrected QT Interval Prolongation. "Corrected QT (QTc) prolongation is predictive of cardiovascular mortality. Frequent occurrence of QT interval prolongation have been found in HIV-positive patients."

@dbdugger - Daniel Brittain Dugger

You said the virus was nothing like HIV. We'll see how many more people like you destroy. Be proud!

@dbdugger — Daniel Brittain Dugger

Posted - June 17, 2025 at 6:03 PM

Saved - June 18, 2025 at 9:53 AM

reSee.it AI Summary

I’ve been reflecting on the parallels between Long COVID and ME/CFS, particularly in how children are suffering. A recent letter from a young girl highlights the urgent need for support. I feel betrayed by academia and advocacy groups for neglecting both Long COVID and HIV+ communities. My research points to significant overlaps in neurocognitive impairments and quality of life issues. The Tat protein's role in both HIV and COVID-19 raises concerns about the long-term effects on health. It’s frustrating to see the lack of action and understanding in addressing these complex illnesses.

@dbdugger - Daniel Brittain Dugger

Victoria, your country drew parallels to ME/CFS. You can give up! Better luck next time.

@acrossthemersey - Jammer

‘Children deserve more than our sympathy, they deserve our urgent action.’ After reading a letter from a 12 year old girl describing her constant pain and only managing 1 hour of school per day, MP Victoria Collins calls for urgent support for UK children living with LongCOVID.

@dbdugger - Daniel Brittain Dugger

In drawing parallels to ME/CFS not only have those in academia, the medical establishment, and "advocacy" groups betrayed the Long Covid population, they have once again betrayed the HIV+ who they supposedly care about, leaving us to worry about our family members.

@dbdugger - Daniel Brittain Dugger

They were so quick to lie to me and others stating the virus was nothing like HIV. Fortunately, I have been around criminals long enough as a bondsman that I don't trust others and certainly don't after reading.

@dbdugger - Daniel Brittain Dugger

Because of my reading over the past three years, I can easily point to three differences: Asymptomatic Neurocognitive Impairment Conversion, Arrythmias leading to death, and AIDS Defining Illness presentation.

@dbdugger - Daniel Brittain Dugger

I can also easily explain why an untold number of children have the Quality of Life of a Cystic Fibrosis patient. Ironically, one protein coursing through their bodies contributes to each of the above and proves their betrayal.

@dbdugger - Daniel Brittain Dugger

That protein is Protein E and it has consistently proven to operate mechanistically as HIV's Tat. SARS-CoV-2 targets ribosomal RNA biogenesis https://www.cell.com/cell-reports/pdf/S2211-1247(24)00219-5.pdf

@dbdugger - Daniel Brittain Dugger

"Finally, the Tat protein of human immunodeficiency virus interacts with FBL and U3 snoRNA, impairing prerRNA processing and depleting mature ribosomes."

@dbdugger - Daniel Brittain Dugger

Soon it will be three years since my drawing attention to the fact individuals suffer from Asymptomatic Neurocognitive Impairment. https://www.linkedin.com/pulse/focusing-cfr-proving-fatal-mistake-daniel-dugger/?trackingId=DX56WPzBS6iWBPD77MGhQQ%3D%3D

Focusing On The CFR Is Proving To Be A Fatal Mistake Since the beginning of the SARS-Cov-2 pandemic, epidemiologists have regularly mentioned what is referred to as the Case Fatality Rate, that is the number of individuals who have been diagnosed with a disease and later die. Large numbers of individuals have used the roughly one percent CFR to relax linkedin.com

@dbdugger - Daniel Brittain Dugger

I did so after reading this article from January of 2022. January 18, 2022 Cerebrospinal Fluid Offers Clues to Post-COVID ‘Brain Fog’ https://www.ucsf.edu/news/2022/01/422156/cerebrospinal-fluid-offers-clues-post-covid-brain-fog

@dbdugger - Daniel Brittain Dugger

"All participants underwent an in-person cognitive testing battery with a neuropsychologist, applying equivalent criteria used for HIV-associated neurocognitive disorder (HAND)."

@dbdugger - Daniel Brittain Dugger

"Surprisingly, the researchers found that 13 of the 22 participants (59 percent) with cognitive symptoms met HAND criteria, compared with seven of the 10 control participants (70 percent)."

@dbdugger - Daniel Brittain Dugger

In order for those in the control arm to be diagnosed with Asymptomatic Neurocognitive Impairment, their ability to complete their Activities of Daily Living had to be preserved, it is not in ME/CFS.

@dbdugger - Daniel Brittain Dugger

HIV-associated neurocognitive disorder — pathogenesis and prospects for treatment https://pmc.ncbi.nlm.nih.gov/articles/PMC4937456/

@dbdugger - Daniel Brittain Dugger

See? Asymptomatic neurocognitive impairment (ANI) Impairment in ≥2 neurocognitive domains (≥1 SD) Does not interfere with daily functioning

@dbdugger - Daniel Brittain Dugger

Could You Have ME/CFS? (Myalgic Encephalomyelitis/Chronic Fatigue Syndrome) https://www.cdc.gov/me-cfs/pdfs/could-you-have-mecfs_508.pdf

@dbdugger - Daniel Brittain Dugger

ME/CFS is a complex illness and symptoms of ME/CFS may seem similar to many other illnesses. ME/CFS requires three symptoms:

@dbdugger - Daniel Brittain Dugger

1. Not being able to participate in routine activities that were possible before becoming ill, such as work, school, social life, and/or personal life, that:

@dbdugger - Daniel Brittain Dugger

In addition, at least one of the following symptoms is also required: Impaired memory or ability to concentrate. People with ME/CFS may have trouble remembering, learning new things, concentrating, or making decisions.

@dbdugger - Daniel Brittain Dugger

Those in Australia have provided two opportunities to point out what I refer to as legalized child abuse. Large hippocampus detected in Long COVID and ME/CFS patients https://news.griffith.edu.au/2025/02/11/large-hippocampus-detected-in-long-covid-and-me-cfs-patients/

Large hippocampus detected in Long COVID and ME/CFS patients - Griffith News Striking brain similarities have been detected in patients who experience Long COVID and Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS), in news.griffith.edu.au

@dbdugger - Daniel Brittain Dugger

Only one population is experiencing the destruction of their hippocampus in the exact same way observed in the HIV+ and that they are was reported last year.

@dbdugger - Daniel Brittain Dugger

2024 Jun 7 SARS-CoV-2 Viroporin E Induces Ca2+ Release and Neuron Cell Death in Primary Cultures of Rat Hippocampal Cells Aged In Vitro https://pmc.ncbi.nlm.nih.gov/articles/PMC11203731/

@dbdugger - Daniel Brittain Dugger

"Highly infectious viruses such as the human immunodeficiency virus (HIV), Ebola virus, or hepatitis C virus encode proteins that function as ion channels."

@dbdugger - Daniel Brittain Dugger

If the suggestion individuals would develop the functional equivalent of HIV Associated Neurocognitive Decline rings a bell, it is that very thing Kenneth Podell predicted almost five years ago.

@dbdugger - Daniel Brittain Dugger

Epub 2020 Sep 29. Multiple Neuroinvasive Pathways in COVID-19 https://pubmed.ncbi.nlm.nih.gov/32990925/

@dbdugger - Daniel Brittain Dugger

Same Tat as above. Same hippocampus. Same Ca2+ overload. HIV-1 protein Tat induces apoptosis of hippocampal neurons by a mechanism involving caspase activation, calcium overload, and oxidative stress https://pubmed.ncbi.nlm.nih.gov/9878167/

@dbdugger - Daniel Brittain Dugger

For reasons only known to them, those in academia, the medical establishment, and "advocacy" groups also turned a blind eye to nineteen years of ME/CFS research, unwilling to treat those with Long Covid as they did with fibromyalgia patients in 2008.

@dbdugger - Daniel Brittain Dugger

Short QT interval https://me-pedia.org/wiki/Short_QT_interval

Short qt interval me-pedia.org

@dbdugger - Daniel Brittain Dugger

2006, Shortened QT interval: a distinctive feature of the dysautonomia of chronic fatigue syndrome. "CONCLUSIONS: Relative short QTc intervals are features of the CFS-related dysautonomia. The significance of this finding is discussed."

@dbdugger - Daniel Brittain Dugger

See? 2008, Electrocardiographic QT interval and cardiovascular reactivity in fibromyalgia differ from chronic fatigue syndrome. "CONCLUSION: A relatively short QTc and positive HIS characterize CFS patients and distinguish them from FM patients. These data may support the contention that FM and CFS are separate disorders."

@dbdugger - Daniel Brittain Dugger

2012, Shortened QTc interval in chronic fatigue syndrome Here we assessed QTc in a large UK population of CFS patients using automated, clinically applicable, measurement techniques and confirmed that QTc is significantly shortened in CFS patients...

@dbdugger - Daniel Brittain Dugger

It was in 2021 that we learned Corrected QT Interval Prolongation is observed with SARS-Cov-2 as it is with HIV. COVID-19 Infection and Corrected QT Interval Prolongation—Collateral Damage From Our Newest Enemy https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2779057

@dbdugger - Daniel Brittain Dugger

Same Tat as above. Same Corrected QT Interval Prolongation. The role of HIV Tat protein in HIV-related cardiovascular diseases https://pmc.ncbi.nlm.nih.gov/articles/PMC5941636/

@dbdugger - Daniel Brittain Dugger

"Corrected QT (QTc) prolongation is predictive of cardiovascular mortality. Frequent occurrence of QT interval prolongation have been found in HIV-positive patients."

@dbdugger - Daniel Brittain Dugger

It was in 2021 that Lucinda Bateman spoke to those unwilling to listen that those living with ME/CFS do not develop what are AIDS Defining Illnesses. Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Essentials of Diagnosis and Management https://www.mayoclinicproceedings.org/article/S0025-6196(21)00513-9/fulltext

@dbdugger - Daniel Brittain Dugger

"Although patients with ME/CFS do not present with symptomatic, opportunistic infections (eg, cryptosporidiosis, tuberculosis), some do experience recurrent herpes infections."

@dbdugger - Daniel Brittain Dugger

6 June 2025 Farm day visitors warned over Cryptosporidium parasite threat https://www.bbc.com/news/articles/cy5e1wn6n22o

Cryptosporidium: Open farm day visitors warned over parasite risk A public health warning is issued as 190,000 people are expected at open farm events across the UK. bbc.com

@dbdugger - Daniel Brittain Dugger

"Tens of thousands of visitors due to attend a UK-wide open farm day this weekend have been warned about a parasitic infection that causes serious gastrointestinal illness."

@dbdugger - Daniel Brittain Dugger

They also have a TB problem. Tuberculosis cases in England continued to increase in 2024 https://www.gov.uk/government/news/tuberculosis-cases-in-england-continued-to-increase-in-2024

Tuberculosis cases in England continued to increase in 2024 UK TB cases rise 13% in 2024, continuing upward trend. gov.uk

@dbdugger - Daniel Brittain Dugger

Timmy, Johnny, Sally, Sammy, and Jimmy were deemed undeserving of the science behind the Estimated Date Of Seroconversion and their fathers were concerned about an Estimated Date of an AIDS Death this Father's Day.

@dbdugger - Daniel Brittain Dugger

Gastro cases hit 20-year high as parasite spreads disease to toddlers https://www.smh.com.au/national/gastro-cases-hit-20-year-high-as-parasite-spreads-disease-to-toddlers-20240702-p5jqjy.html

Gastro cases hit 20-year high as parasite spreads disease to toddlers A gastrointestinal disease caused by the cryptosporidiosis parasite has reached alarming rates, with daycare and school aged children picking up the infection. smh.com.au

@dbdugger - Daniel Brittain Dugger

"There have been 11,747 cryptosporidiosis cases in 2024 compared with 3716 in 2023. A quarter of all cases are in children under four."

@dbdugger - Daniel Brittain Dugger

Same Tat as above. Same Cryptosporidium Parvum as above. HIV-1 Tat Protein Suppresses Cholangiocyte Toll-Like Receptor 4 Expression and Defense against Cryptosporidium parvum https://pmc.ncbi.nlm.nih.gov/articles/PMC2716168/

HIV-1 Tat Protein Suppresses Cholangiocyte Toll-Like Receptor 4 Expression and Defense against Cryptosporidium parvum Biliary cryptosporidiosis is associated with acquired immunodeficiency syndrome (AIDS) cholangiopathy and occurs almost exclusively in adult patients with AIDS. Infection of biliary epithelial cells (cholangiocytes) with Cryptosporidium parvum ... pmc.ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

Reported this year is that many have the Quality of Life of a Cystic Fibrosis patient. Long COVID Is Fueling a Mental Health Crisis in Children https://www.unmc.edu/healthsecurity/transmission/2025/05/28/long-covid-is-fueling-a-mental-health-crisis-in-children/

Long COVID Is Fueling a Mental Health Crisis in Children Neuroscience News A new study reveals that nearly 40% of children with long COVID are experiencing significant symptoms of anxiety or depression, many for the first time. Using validated mental hea… unmc.edu

@dbdugger - Daniel Brittain Dugger

"These children reported a quality of life comparable to peers with serious illnesses like cancer or cystic fibrosis, with many expressing a deep sense of ineffectiveness and loss of confidence."

@dbdugger - Daniel Brittain Dugger

It was reported in 2021 that increased TGF-b signaling is observed. SARS-CoV-2 in severe COVID-19 induces a TGF-β-dominated chronic immune response that does not target itself https://www.nature.com/articles/s41467-021-22210-3

SARS-CoV-2 in severe COVID-19 induces a TGF-β-dominated chronic immune response that does not target itself - Nature Communications The pathogenesis of severe COVID-19 reflects an inefficient immune reaction to SARS-CoV-2. Here we analyze, at the single cell level, plasmablasts egressed into the blood to study the dynamics of adaptive immune response in COVID-19 patients requiring intensive care. Before seroconversion in response to SARS-CoV-2 spike protein, peripheral plasmablasts display a type 1 interferon-induced gene expression signature; however, following seroconversion, plasmablasts lose this signature, express instead gene signatures induced by IL-21 and TGF-β, and produce mostly IgG1 and IgA1. In the sustained immune reaction from COVID-19 patients, plasmablasts shift to the expression of IgA2, thereby reflecting an instruction by TGF-β. Despite their continued presence in the blood, plasmablasts are not found in the lungs of deceased COVID-19 patients, nor does patient IgA2 binds to the dominant antigens of SARS-CoV-2. Our results thus suggest that, in severe COVID-19, SARS-CoV-2 triggers a chronic immune reaction that is instructed by TGF-β, and is distracted from itself. Our understanding on the humoral immunity induced by SARS-CoV-2 is still lacking. Here the authors analyze B cell responses at the single cell level to find that, in severe COVID-19 patients, plasmablasts shift from IFN to TGFβ instruction to produce IgA antibodies that are not specific to dominant SARS-CoV-2 antigens. nature.com

@dbdugger - Daniel Brittain Dugger

Were I experiencing the silencing of the Cystic Fibrosis Transmembrane Conductance Receptor, I too would have the Quality of Life of a CF patient. Inflammation in the COVID-19 airway is due to inhibition of CFTR signaling by the SARS-CoV-2 spike protein https://www.nature.com/articles/s41598-024-66473-4

Inflammation in the COVID-19 airway is due to inhibition of CFTR signaling by the SARS-CoV-2 spike protein - Scientific Reports SARS-CoV-2-contributes to sickness and death in COVID-19 patients partly by inducing a hyper-proinflammatory immune response in the host airway. This hyper-proinflammatory state involves activation of signaling by NFκB, and unexpectedly, ENaC, the epithelial sodium channel. Post-infection inflammation may also contribute to "Long COVID"/PASC. Enhanced signaling by NFκB and ENaC also marks the airway of patients suffering from cystic fibrosis, a life-limiting proinflammatory genetic disease due to inactivating mutations in the CFTR gene. We therefore hypothesized that inflammation in the COVID-19 airway might similarly be due to inhibition of CFTR signaling by SARS-CoV-2 spike protein, and therefore activation of both NFκB and ENaC signaling. We used western blot and electrophysiological techniques, and an organoid model of normal airway epithelia, differentiated on an air–liquid-interface (ALI). We found that CFTR protein expression and CFTR cAMP-activated chloride channel activity were lost when the model epithelium was exposed to SARS-CoV-2 spike proteins. As hypothesized, the absence of CFTR led to activation of both TNFα/NFκB signaling and α and γ ENaC. We had previously shown that the cardiac glycoside drugs digoxin, digitoxin and ouabain blocked interaction of spike protein and ACE2. Consistently, addition of 30 nM concentrations of the cardiac glycoside drugs, prevented loss of both CFTR protein and CFTR channel activity. ACE2 and CFTR were found to co-immunoprecipitate in both basal cells and differentiated epithelia. Thus spike-dependent CFTR loss might involve ACE2 as a bridge between Spike and CFTR. In addition, spike exposure to the epithelia resulted in failure of endosomal recycling to return CFTR to the plasma membrane. Thus, failure of CFTR recovery from endosomal recycling might be a mechanism for spike-dependent loss of CFTR. Finally, we found that authentic SARS-CoV-2 virus infection induced loss of CFTR protein, which was rescued by the cardiac glycoside drugs digitoxin and ouabain. Based on experiments with this organoid model of small airway epithelia, and comparisons with 16HBE14o- and other cell types expressing normal CFTR, we predict that inflammation in the COVID-19 airway may be mediated by inhibition of CFTR signaling by the SARS-CoV-2 spike protein, thus inducing a cystic fibrosis-like clinical phenotype. To our knowledge this is the first time COVID-19 airway inflammation has been experimentally traced in normal subjects to a contribution from SARS-CoV-2 spike-dependent inhibition of CFTR signaling. nature.com

@dbdugger - Daniel Brittain Dugger

Same Tat as above. Same TGF-b as above. Same CFTR silencing as above. HIV Tat Protein Induces the TGF-β Signaling Pathway and Suppresses the CFTR Biogenesis and Activity by microRNA-Regulated Gene-Silencing Mechanism https://faseb.onlinelibrary.wiley.com/doi/abs/10.1096/fasebj.2020.34.s1.00650

@dbdugger - Daniel Brittain Dugger

For those who don't give up, let me assuage your fears. PEM is not observed in exercises in futility, like trying to save those you destroyed due to your mental weakness and moral bankruptcy. For that, you should rejoice.

@dbdugger — Daniel Brittain Dugger

Posted - June 16, 2025 at 12:30 PM

Saved - June 16, 2025 at 11:59 PM

reSee.it AI Summary

I discuss the ongoing challenges faced by individuals with ALS, referencing Dane's struggles with losing motor function. I express skepticism about the reliability of medical devices and mock those who have dismissed the severity of neurocognitive impairments. I highlight research linking COVID-19 to cognitive issues and the role of TDP-43 in various neurodegenerative diseases. I also draw parallels between HIV and SARS-CoV-2, emphasizing the neurotoxic effects of their proteins. Lastly, I critique those who underestimate the seriousness of these conditions.

@dbdugger - Daniel Brittain Dugger

As with ME/CFS, efforts to Solve ALS continue to this day, that's why you don't allow individuals to experience Vpu-like mediated neurological damage which includes the cleavage of TDP-43. Weirdos. Losers. LMAO!

@BirdieBittern - BirdieBittern

After first revealing his ALS in April, Dane said he has lost function of his right arm & worries about what's next. "I feel like maybe a couple, few more months, & I won't have my left-hand functioning either" & is worried about the loss of his legs. https://abcnews.go.com/GMA/Culture/eric-dane-opens-als-diagnosis-end-story/story?id=122809085

Eric Dane says he has lost use of his right arm amid ALS battle Dane opened up about his health battle with ABC News' Diane Sawyer. abcnews.go.com

@dbdugger - Daniel Brittain Dugger

It appears we decided to run a wheel off and I can only hope the same doesn't happen to his wheelchair. Surely, the wheelchair manufacturer won't betray him as those who drew parallels to ME/CFS did.

@dbdugger - Daniel Brittain Dugger

I might as well take the opportunity to laugh, mock, and ridicule those who cared so little about him that they allowed for his conversion from Asymptomatic Neurocognitive Impairment, observed in seventy percent of Dr. Apple's control arm.

@dbdugger - Daniel Brittain Dugger

Cerebrospinal Fluid Offers Clues to Post-COVID ‘Brain Fog’ https://www.ucsf.edu/news/2022/01/422156/cerebrospinal-fluid-offers-clues-post-covid-brain-fog

@dbdugger - Daniel Brittain Dugger

"All participants underwent an in-person cognitive testing battery with a neuropsychologist, applying equivalent criteria used for HIV-associated neurocognitive disorder (HAND)."

@dbdugger - Daniel Brittain Dugger

"Surprisingly, the researchers found that 13 of the 22 participants (59 percent) with cognitive symptoms met HAND criteria, compared with seven of the 10 control participants (70 percent)."

@dbdugger - Daniel Brittain Dugger

Will be interesting to see if the mutation in ORF3a contributes to an acceleration of the cleavage of TDP-43. PQ.2+Orf3a:I20T(34 seqs, >10 places, 10% Hong Kong) https://github.com/cov-lineages/pango-designation/issues/2954

PQ.2+Orf3a:I20T(34 seqs, >10 places, 10% Hong Kong) · Issue #2954 · cov-lineages/pango-designation From sars-cov-2-variants/lineage-proposals#2559 NB.1.8.1 seems to be getting the SARS-1 Orf3a:193R mutation. According to @ryhisner, ORF3a:W193 is a key residue. The SARS-CoV-1 ORF3a seems to function very differently than the SARS-CoV-2... github.com

@dbdugger - Daniel Brittain Dugger

HIV's Vpu does appear in the title along with SARS-Cov-2's ORF3a, correct? HIV-1 Vpu and SARS-CoV-2 ORF3a proteins disrupt STING-mediated activation of antiviral NF-κB signaling https://www.science.org/doi/10.1126/scisignal.add6593

@dbdugger - Daniel Brittain Dugger

We have only known of the productive infection of the very cell type whose dysregulation leads to premature brain aging, Alzheimer's, Parkinson's, and Amyotrophic Lateral Sclerosis since 2021.

@dbdugger - Daniel Brittain Dugger

Microglial Implications in SARS-CoV-2 Infection and COVID-19: Lessons From Viral RNA Neurotropism and Possible Relevance to Parkinson’s Disease https://www.frontiersin.org/journals/cellular-neuroscience/articles/10.3389/fncel.2021.670298/full

Frontiers | Microglial Implications in SARS-CoV-2 Infection and COVID-19: Lessons From Viral RNA Neurotropism and Possible Relevance to Parkinson’s Disease Since December 2019, humankind has been experiencing a ravaging severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) outbreak, the second coronavirus... frontiersin.org

@dbdugger - Daniel Brittain Dugger

We have only known of the cleavage of TDP-43 since 2023. Published: 09 March 2023 The SARS-CoV-2 main protease induces neurotoxic TDP-43 cleavage and aggregates https://www.nature.com/articles/s41392-023-01386-8

The SARS-CoV-2 main protease induces neurotoxic TDP-43 cleavage and aggregates - Signal Transduction and Targeted Therapy nature.com

@dbdugger - Daniel Brittain Dugger

"TAR DNA-binding protein (TDP-43) is a primary component of insoluble aggregates associated with several devastating nervous system disorders, including amyotrophic lateral sclerosis (ALS) and multiple forms of frontotemporal lobar degeneration (FTLD)."

@dbdugger - Daniel Brittain Dugger

Same Vpu. Same TDP-43. HIV-1 Vpu induces neurotoxicity by promoting Caspase 3-dependent cleavage of TDP-43 https://www.embopress.org/doi/full/10.1038/s44319-024-00238-y?af=R

@dbdugger - Daniel Brittain Dugger

Those who said it was nothing like HIV won't have to worry about buying Halloween costumes for their children. They'll be able to go as Stephen Hawkins minus his cognition. https://t.co/rq8I7m0h34

@dbdugger — Daniel Brittain Dugger

Posted - June 6, 2024 at 9:08 AM

Saved - June 7, 2024 at 8:55 PM

reSee.it AI Summary

Children with long COVID experience persistent symptoms, leading to increased school absences. SARS-CoV-2 depletes CD4 cells, similar to HIV, and can directly attack the brain, causing long-term cognitive impairment. The virus infects various cell types in the central nervous system, contributing to neurodegenerative diseases. Drug repurposing and understanding the virus's mechanisms are crucial for treatment. The parallels drawn to ME/CFS neglect the unique challenges and consequences of a chronic SARS-CoV-2 infection.

@dbdugger - Daniel Brittain Dugger

Why? Their brains, livers, kidneys, and immune systems have been durned up by those who deprived them of forty years of evidenced based medicine, drawing parallels to ME/CFS.

@LongCovidHell - Dame Sa 🐝 3.5%

Why are school absences so high? Why are so many kids sick? “…some children develop #LongCOVID and experience persistent or intermittent symptoms that reduces their quality of life. This can result in increased school absences…” #LongCovidKids #Schools https://www.nationalacademies.org/news/2024/06/new-report-reviews-evidence-on-long-covid-diagnosis-risk-symptoms-and-functional-impact-for-patients

New Report Reviews Evidence on Long COVID Diagnosis, Risk, Symptoms, and Functional Impact for Patients A new National Academies report for the Social Security Administration presents findings about Long COVID, including that it can cause more than 200 symptoms and that some effects can impact an individual’s ability to function for six months to two years or longer after COVID-19 infection. nationalacademies.org

@dbdugger - Daniel Brittain Dugger

Didn't have to happen, as we were prepared to preserve their autonomy, immune competence, and cognition.

@dbdugger - Daniel Brittain Dugger

Not the first time we have observed a virus that depletes CD4 cells, it is persistent, there is an aversion to non-pharmaceutical interventions, vaccines are not protective, and there is forward transmission.

@dbdugger - Daniel Brittain Dugger

That it would be prudent to borrow from forty years of evidenced based medicine was made known on September 28th and 29th, 2020.

@dbdugger - Daniel Brittain Dugger

On September 28th, 2020 it became known that SARS-Cov-2 depletes the CD4 compartment, as does HIV. SARS-CoV-2 Uses CD4 to Infect T Helper Lymphocytes https://www.medrxiv.org/content/10.1101/2020.09.25.20200329v1

SARS-CoV-2 Uses CD4 to Infect T Helper Lymphocytes medRxiv - The Preprint Server for Health Sciences medrxiv.org

@dbdugger - Daniel Brittain Dugger

On September 29th, 2020, Kenneth Podell suggested individuals would be living with the functional equivalent of HIV Associated Neurocognitive Decline. Oh, no. Not the big scary word HIV.

@dbdugger - Daniel Brittain Dugger

Multiple Neuroinvasive Pathways in COVID-19 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7523266/

Multiple Neuroinvasive Pathways in COVID-19 COVID-19 is a highly infectious viral disease caused by the novel coronavirus SARS-CoV-2. While it was initially regarded as a strictly respiratory illness, the impact of COVID-19 on multiple organs is increasingly recognized. The brain is among the targets ... ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

"However, it did not take long to discover that the disease could also attack the brain directly, which resulted in long-term cognitive impairment."

@dbdugger - Daniel Brittain Dugger

Subsequent journal articles would prove his prescience.

@dbdugger - Daniel Brittain Dugger

In December of 2021, Dr. Daniel Chertow implicated the two most well known reservoirs in HIV, that of the Central Nervous System and Gut Associated Lymphoid Tissues. SARS-CoV-2 infection and persistence throughout the human body and brain https://assets.researchsquare.com/files/rs-1139035/v1_covered.pdf?c=1640020576

@dbdugger - Daniel Brittain Dugger

Despite the well known challenges associated with their involvement, no effort has been made to engage in drug repurposing to militate against profound reservoir seeding.

@dbdugger - Daniel Brittain Dugger

We could have beaten China to the punch with the repurposing as the efficacy of TDF was suggested months before they repurposed Azvudine in December of 2021.

@dbdugger - Daniel Brittain Dugger

May, 2021 Tenofovir, Another Inexpensive, Well-Known and Widely Available Old Drug Repurposed for SARS-COV-2 Infection https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8150375/

Tenofovir, Another Inexpensive, Well-Known and Widely Available Old Drug Repurposed for SARS-COV-2 Infection Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is spreading worldwide with different clinical manifestations. Age and comorbidities may explain severity in critical cases and people living with human immunodeficiency virus (HIV) ... ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

While Chertow did not implicate individual cell types productively infected by SARS-Cov-2, others certainly have. The Central Nervous System Reservoir of those living with HIV and SARS-Cov-2 are indistinguishable as far as cell type involvement.

@dbdugger - Daniel Brittain Dugger

2022 Jul 18 In SARS-CoV-2, astrocytes are in it for the long haul https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9335203/

In SARS-CoV-2, astrocytes are in it for the long haul ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

In Astrocytes are HIV reservoirs in the brain: A cell type with poor HIV infectivity and replication but efficient cell-to-cell viral transfer, the authors determined that astrocytes are a reservoir of latent virus.

@dbdugger - Daniel Brittain Dugger

Astrocytes are HIV reservoirs in the brain: a cell type with poor HIV-infectivity and replication but efficient cell-to-cell viral transfer. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11102126/

Astrocytes are HIV reservoirs in the brain: a cell type with poor HIV-infectivity and replication but efficient cell-to-cell viral transfer The major barrier to eradicating HIV-infection is the generation of tissue-associated quiescent long-lasting viral reservoirs refractory to therapy. Upon interruption of antiretroviral therapy (ART), it can be reactivated. Within the brain, microglia/macrophages ... ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

When TNF-alpha is elevated, an individual experiences shortness of breath, a down-regulation in BDNF that prevents the formation of new synapses, a reactivation of astrocytes which allows for cell-to-cell transfer into those cells which allow for high viral replication.

@dbdugger - Daniel Brittain Dugger

Beyond serving as a reservoir for latent virus, their involvement comes with other significant complications, as is explained in Astrocytes, HIV and the Glymphatic System: A Disease of Disrupted Waste Management?

@dbdugger - Daniel Brittain Dugger

Astrocytes, HIV and the Glymphatic System: A Disease of Disrupted Waste Management. https://pubmed.ncbi.nlm.nih.gov/33134185/

Astrocytes, HIV and the Glymphatic System: A Disease of Disrupted Waste Management? - PubMed The discovery of the glial-lymphatic or glymphatic fluid clearance pathway in the rodent brain led researchers to search for a parallel system in humans and to question the implications of this pathway in neurodegenerative diseases. Magnetic resonance imaging studies revealed that several features o … pubmed.ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

Representing thirty percent of the cells within the Central Nervous System, they participate in maintaining homeostasis and providing trophic support of neurons.

@dbdugger - Daniel Brittain Dugger

Astrocytes of the A1 phenotype are observed in a number of neurodegenerative disorders including HIV Associated Neurocognitive Decline, Parkinson's Disease, Epilepsy, Traumatic Brain Injury, and Alzheimer's Disease. Their presence is indicative of a neurotoxic environment.

@dbdugger - Daniel Brittain Dugger

When the environment becomes ischemic, or there is a reduction in blood flow, the A2 phenotype can be found. Both the A1 and A2 phenotype contribute to impaired glymphatic system involvement, leading to inflammation and the accumulation of toxic waste products.

@dbdugger - Daniel Brittain Dugger

In concert with microglia, astrocytes exert a "bystander" effect on oligodendrocytes, responsible for the production of myelin.

@dbdugger - Daniel Brittain Dugger

Macrophages and Monocytes: “Trojan Horses” in COVID-19 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8624282/

@dbdugger - Daniel Brittain Dugger

Like with HIV, monocytes that have been productively infected by SARS-Cov-2 are trafficked into the Central Nervous System of individuals living with SARS-Cov-2 Associated Neurocognitive Decline.

@dbdugger - Daniel Brittain Dugger

Once within the Central Nervous System, the monocytes differentiate into what are referred to as perivascular macrophages, in the event they were programmed to become such.

@dbdugger - Daniel Brittain Dugger

Perivascular macrophages are the primary cell type productively infected by simian immunodeficiency virus in the brains of macaques: implications for the neuropathogenesis of AIDS - PubMed The macrophage is well established as a target of HIV and simian immunodeficiency virus (SIV) infection and a major contributor to the neuropathogenesis of AIDS. However, the identification of distinct subpopulations of monocyte/macrophages that carry virus to the brain and that sustain infection wi … pubmed.ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

Perivascular macrophages are a major cell type that is productively infected when the viral load is at its highest.

@dbdugger - Daniel Brittain Dugger

The biology of perivascular macrophages is unique in that they rapidly turnover and replaced by peripheral blood monocytes/macrophages. It is believed they contribute to the appearance and disappearance of virus within the Central Nervous System.

@dbdugger - Daniel Brittain Dugger

Dysregulation of brain and choroid plexus cell types in severe COVID-19 https://www.nature.com/articles/s41586-021-03710-0

Dysregulation of brain and choroid plexus cell types in severe COVID-19 - Nature Although SARS-CoV-2 primarily targets the respiratory system, patients with and survivors of COVID-19 can suffer neurological symptoms1–3. However, an unbiased understanding of the cellular and molecular processes that are affected in the brains of patients with COVID-19 is missing. Here we profile 65,309 single-nucleus transcriptomes from 30 frontal cortex and choroid plexus samples across 14 control individuals (including 1 patient with terminal influenza) and 8 patients with COVID-19. Although our systematic analysis yields no molecular traces of SARS-CoV-2 in the brain, we observe broad cellular perturbations indicating that barrier cells of the choroid plexus sense and relay peripheral inflammation into the brain and show that peripheral T cells infiltrate the parenchyma. We discover microglia and astrocyte subpopulations associated with COVID-19 that share features with pathological cell states that have previously been reported in human neurodegenerative disease4–6. Synaptic signalling of upper-layer excitatory neurons—which are evolutionarily expanded in humans7 and linked to cognitive function8—is preferentially affected in COVID-19. Across cell types, perturbations associated with COVID-19 overlap with those found in chronic brain disorders and reside in genetic variants associated with cognition, schizophrenia and depression. Our findings and public dataset provide a molecular framework to understand current observations of COVID-19-related neurological disease, and any such disease that may emerge at a later date. Single-nucleus transcriptomes of frontal cortex and choroid plexus samples from patients with COVID-19 reveal pathological cell states that are similar to those associated with human neurodegenerative diseases and chronic brain disorders. nature.com

@dbdugger - Daniel Brittain Dugger

The choroid plexus is yet another example of Central Nervous System Reservoir resident macrophage and responsible for the production of cerebrospinal fluid.

@dbdugger - Daniel Brittain Dugger

Like meningeal macrophages, they are not considered major targets for productive infection. With that said, it has been proven that they are, with individuals developing hydrocephalus secondary to their chronic SARS-Cov-2 infection.

@dbdugger - Daniel Brittain Dugger

Hydrocephalus secondary to COVID-19 infection. https://academic.oup.com/qjmed/article/116/7/559/7082960

@dbdugger - Daniel Brittain Dugger

As is observed with HIV, SARS-Cov-2 productively infects brain pericytes, known to not only harbor latent virus but contribute to Cerebral Blood Flow disturbances and Blood Brain Barrier degradation.

@dbdugger - Daniel Brittain Dugger

Infection of Brain Pericytes Underlying Neuropathology of COVID-19 Patients https://pubmed.ncbi.nlm.nih.gov/34769052/

@dbdugger - Daniel Brittain Dugger

Both SARS-Cov-2 and HIV productively infect microglia, the resident immune cell within the CNS and that which constitutes the primary cell type comprising the CNS reservoir.

@dbdugger - Daniel Brittain Dugger

SARS-CoV-2 Infection of Microglia Elicits Proinflammatory Activation and Apoptotic Cell Death https://pubmed.ncbi.nlm.nih.gov/35510852/

SARS-CoV-2 Infection of Microglia Elicits Proinflammatory Activation and Apoptotic Cell Death - PubMed Accumulating evidence suggests that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection causes various neurological symptoms in patients with coronavirus disease 2019 (COVID-19). The most dominant immune cells in the brain are microglia. Yet, the relationship between neurological … pubmed.ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

Microglial Cells: The Main HIV-1 Reservoir in the Brain https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6821723/

Microglial Cells: The Main HIV-1 Reservoir in the Brain Despite efficient combination of the antiretroviral therapy (cART), which significantly decreased mortality and morbidity of HIV-1 infection, a definitive HIV cure has not been achieved. Hidden HIV-1 in cellular and anatomic reservoirs is the major hurdle ... ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

Microglial involvement brings a number of challenges. First, they are believed to contribute to the emergence of therapeutic resistant strains through "CNS Escape."

@dbdugger - Daniel Brittain Dugger

Second, they contribute to a number of neurodegenerative diseases, the predisposition to same compounded by pathophysiological processes described in other journal articles.

@dbdugger - Daniel Brittain Dugger

As a consequence of their dysregulation and amyloid deposition known since 2022, an untold number are predisposed to Alzheimer's. Amyloidogenesis of SARS-CoV-2 Spike Protein https://pubs.acs.org/doi/10.1021/jacs.2c03925

@dbdugger - Daniel Brittain Dugger

As a consequence of their dysregulation and basal ganglia persistence, observed by Chertow in 2021, and to which the substantia nigra belongs and is responsible for the production of dopamine, an untold are predisposed to Parkinson's.

@dbdugger - Daniel Brittain Dugger

Finally, their dysregulation leads to Amyotrophic Lateral Sclerosis.

@dbdugger - Daniel Brittain Dugger

Among the cell types resistant to apoptosis, or death, their clearance will require a Latency Reversal Agent to "Shock & Kill" or Latency Promoting Agent to "Lock & Block."

@dbdugger - Daniel Brittain Dugger

Absolutely ridiculous for anyone to believe that 1 billion a year will accomplish what hasn't been done in forty years with a budget of 3 billion. Neither exist.

@dbdugger - Daniel Brittain Dugger

Unfortunately, academia, the medical establishment, and "advocacy" groups drew parallels to a condition for which Asymptomatic Neurocognitive Impairment is not observed, a Treatment as Prevention strategy does not exist, proteins do not operate as HIV's, and TB doesn't reactivate

@dbdugger - Daniel Brittain Dugger

Every single day parallels are drawn to ME/CFS, the medical establishment betrays its income source, destroying their immune competence and cognition.

@dbdugger - Daniel Brittain Dugger

In 2022, Ana Pepe demonstrated that the Central Nervous System of those living with a chronic SARS-Cov-2 infection expands through the same mechanism observed in those living with HIV, the Tunneling Nanotube.

@dbdugger - Daniel Brittain Dugger

Tunneling nanotubes provide a route for SARS-CoV-2 spreading https://www.science.org/doi/full/10.1126/sciadv.abo0171

@dbdugger - Daniel Brittain Dugger

She highlights the well known challenges associated with their formation, which is why HIV antivirals are initiated same day in the US.

@dbdugger - Daniel Brittain Dugger

"Several viruses, such as the influenza virus, HIV, and herpes simplex virus (31), can use TNTs to transfer their genomes to naïve cells, a mechanism of direct cell-to-cell communication that allows evasion of host immunity and to avoid pharmaceutical targeting."

@dbdugger - Daniel Brittain Dugger

"This evidence supports our hypothesis that SARS-CoV-2, similar to other viruses such as HIV (30, 72), is an inducer of TNT formation, to facilitate its spreading between TNT-connected cells."

@dbdugger - Daniel Brittain Dugger

"On the basis of our observations, the transfer of SARS-CoV-2 occurs via TNTs through both extracellular adhesion (i.e., surfing) and intracellular transport in agreement with what has been already shown for HIV."

@dbdugger - Daniel Brittain Dugger

"For example, HIV is able to not only “hijack” TNTs but also gap junctional communication to spread toxic signals to uninfected astrocytes."

@dbdugger - Daniel Brittain Dugger

There is in fact a connection between clogged arteries and cognitive impairment, a SARS-Cov-2 protein operating mechanistically as HIV's Nef.

@dbdugger - Daniel Brittain Dugger

SARS-CoV-2 infection triggers pro-atherogenic inflammatory responses in human coronary vessels https://www.nature.com/articles/s44161-023-00336-5

@dbdugger - Daniel Brittain Dugger

Ironically, citation #34 mentions the down regulation of MHC-I, seen in the untreated HIV positive as a consequence of its Nef protein. HIV-1 Nef blocks transport of MHC class I molecules to the cell surface via a PI 3-kinase-dependent pathway https://pubmed.ncbi.nlm.nih.gov/11289809/

HIV-1 Nef blocks transport of MHC class I molecules to the cell surface via a PI 3-kinase-dependent pathway - PubMed HIV causes a chronic infection by evading immune eradication. A key element of HIV immune escape is the HIV-1 Nef protein. Nef causes a reduction in the level of cell surface major histocompatibility complex class I (MHC-I) protein expression, thus protecting HIV-infected cells from anti-HIV cytotox … pubmed.ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

Every single day that parallels continue to be drawn to ME/CFS, there is only one population suffering the consequences of a protein operating mechanistically as HIV's Tat, destroying the eyes, blood vessels, and brains of millions.

@dbdugger - Daniel Brittain Dugger

In the untreated HIV positive, Tat contributes to a number of pathophysiological processes. SARS-CoV-2 targets ribosomal RNA biogenesis https://www.cell.com/cell-reports/fulltext/S2211-1247(24)00219-5

@dbdugger - Daniel Brittain Dugger

"Finally, the Tat protein of human immunodeficiency virus interacts with FBL and U3 snoRNA, impairing pre-rRNA processing and depleting mature ribosomes."

@dbdugger - Daniel Brittain Dugger

Tat and Amyloid deposition within the Central Nervous System leads to cerebrovascular toxicity. HIV-1 Tat-induced cerebrovascular toxicity is enhanced in mice with amyloid deposits https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3206197/

HIV-1 Tat-induced cerebrovascular toxicity is enhanced in mice with amyloid deposits HIV-1-infected brains are characterized by elevated depositions of amyloid beta (Aβ); however, the interactions between Aβ and HIV-1 are poorly understood. In the present study, we administered specific HIV-1 protein Tat into the cerebral ... ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

Tat also contributes to reactive gliosis. Reactive gliosis and neuroinflammation: prime suspects in the pathophysiology of post-acute neuroCOVID-19 syndrome https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10492094/

Reactive gliosis and neuroinflammation: prime suspects in the pathophysiology of post-acute neuroCOVID-19 syndrome As the repercussions from the COVID-19 pandemic continue to unfold, an ever-expanding body of evidence suggests that infection also elicits pathophysiological manifestations within the central nervous system (CNS), known as neurological symptoms of post-acute ... ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

Synaptic transport of human immunodeficiency virus-Tat protein causes neurotoxicity and gliosis in rat brain https://pubmed.ncbi.nlm.nih.gov/12968004/

Synaptic transport of human immunodeficiency virus-Tat protein causes neurotoxicity and gliosis in rat brain - PubMed Neurodegeneration, synaptic alterations, and gliosis are prominent features of human immunodeficiency virus (HIV) encephalitis, but HIV encephalitis is distinct from other viral encephalitides because neurodegeneration occurs in uninfected neurons at anatomical sites that are often distant from the … pubmed.ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

Tat contributes to microglial ferroptosis, implicated in Parkinson's Disease. COVID-19 related neurological manifestations in Parkinson’s disease: has ferroptosis been a suspect? https://www.nature.com/articles/s41420-024-01915-6

COVID-19 related neurological manifestations in Parkinson’s disease: has ferroptosis been a suspect? - Cell Death Discovery A rising number of patient cases point to a probable link between SARS-CoV-2 infection and Parkinson’s disease (PD), yet the mechanisms by which SARS-CoV-2 affects the brain and generates neuropsychiatric symptoms in COVID-19 patients remain unknown. Ferroptosis, a distinct iron-dependent non-apoptotic type of cell death characterized by lipid peroxidation and glutathione depletion, a key factor in neurological disorders. Ferroptosis may have a pathogenic role in COVID-19, according to recent findings, however its potential contributions to COVID-19-related PD have not yet been investigated. This review covers potential paths for SARS-CoV-2 infection of the brain. Among these putative processes, ferroptosis may contribute to the etiology of COVID-19-associated PD, potentially providing therapeutic methods. nature.com

@dbdugger - Daniel Brittain Dugger

HIV-1 Tat-mediated microglial ferroptosis involves the miR-204-ACSL4 signaling axis https://pubmed.ncbi.nlm.nih.gov/37023693/

HIV-1 Tat-mediated microglial ferroptosis involves the miR-204-ACSL4 signaling axis - PubMed This study was focused on exploring the role of the HIV-1 Tat protein in mediating microglial ferroptosis. Exposure of mouse primary microglial cells (mPMs) to HIV-1 Tat protein resulted in induction of ferroptosis, which was characterized by increased expression of Acyl-CoA synthetase long-chain fa … pubmed.ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

Tat destroys the blood retinal barrier. SARS-CoV-2 infects cells lining the blood-retinal barrier and induces a hyperinflammatory immune response in the retina via systemic exposure https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1012156

SARS-CoV-2 infects cells lining the blood-retinal barrier and induces a hyperinflammatory immune response in the retina via systemic exposure Author summary SARS-CoV-2 is known to cause several ocular manifestations in COVID-19 patients; however, the role of eyes in viral transmission and ocular tissue tropism remains elusive. The presence of viral remnants in various ocular tissues and fluids from COVID-19 patients has led to an assumption that SARS-CoV-2 may be transmitted through the eyes. Here, we show that SARS-CoV-2 ocular tropism is through cells lining the BRB. SARS-CoV-2 not only infects the various parts of the eye via systemic exposure but also induces a hyperinflammatory immune and antiviral response in the retina. Unexpectedly, the corneal epithelium was found to be resistant to SARS-CoV-2 infection, and ocular exposure of SARS-CoV-2 failed to cause lung pathology and moribund illness. Cells lining the BRB showed induced expression of viral entry receptors and enhanced susceptibility towards SARS-CoV-2-induced cell death, which is further potentiated with comorbidities such as hyperglycemia. Our findings from this study shed light on the role of BRB in SARS-CoV-2 ocular tropism and the role of eyes in viral transmission. journals.plos.org

@dbdugger - Daniel Brittain Dugger

HIV-1 Tat-Mediated Apoptosis in Human Blood-Retinal Barrier-Associated Cells https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0095420

HIV-1 Tat-Mediated Apoptosis in Human Blood-Retinal Barrier-Associated Cells HIV-1-associated ocular complications, such as microvasculopathies, can lead to the loss of vision in HIV-1-infected patients. Even in patients under highly active antiretroviral therapy, ocular lesions are unavoidable. Ocular complications have been demonstrated to be closely related to the breakdown of the blood-retinal-barrier (BRB); however, the underlying mechanism is not clear. The data from this study indicated that the HIV-1 Tat protein induced the apoptosis of human retinal microvascular endothelial cells (HRMECs) and retinal pigmen epithelium (RPE) cells, which compose the inner BRB and the outer BRB, respectively. In addition, this study found that the activation of N-methyl-D-aspartate receptors (NMDARs) was involved in the apoptosis of RPE cells, but it caused no changes in HRMECs. Furthermore, both cell types exhibited enhanced expression of Bak, Bax and Cytochrome c. The inhibition of Tat activity protected against the apoptosis induced by NMDAR activation and prevented the dysregulation of Bak, Bax and Cytochrome c, revealing an important role for the mitochondrial pathway in HIV-1 Tat-induced apoptosis. Together, these findings suggest a possible mechanism and may identify a potential therapeutic strategy for HIV-1-associated ocular complications. journals.plos.org

@dbdugger - Daniel Brittain Dugger

To further demonstrate the genius of Kenneth Podell, let's look to this document. HIV-1 Encephalopathy and Aids Dementia Complex https://www.ncbi.nlm.nih.gov/books/NBK507700/

HIV-1 Encephalopathy and Aids Dementia Complex Neurocognitive deficits are the presenting complaint in 4% to 15% of patients diagnosed with HIV. Patients may present with nonspecific complaints such as deficits in memory, concentration, attention, and motor skills. These symptoms are common in many disorders, and accurate diagnosis is critical for appropriate treatment. The AIDS dementia complex (ADC) was first defined in 1986. It was a frequent feature of HIV disease before antiretroviral therapy (ART) and highly active antiretroviral therapy (HAART) came into common use in the mid-1990s. In addition to medical comorbidities, patients also frequently suffer from various mental or psychosocial issues that can affect cognitive function, including mood disorders, post-traumatic stress disorder (PTSD), and substance abuse or dependence. Increased risk of opportunistic infections, tumors, and side effects of antiretroviral drugs may also contribute to neurologic effects. Patients can experience delirium as part of the acute HIV syndrome or develop dementia during the later stages of their disease.[1][2] ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

"Dementia, including Parkinson, Alzheimer, Lewy Body, and frontal and temporal lobe dementias."

@dbdugger - Daniel Brittain Dugger

As parallels continue to be drawn to ME/CFS, there is only population living with a persistent infection for which a protein is operating mechanistically as HIV's Vpr. The consequences of such are many, including a-synuclein aggregation, leading to Lewy Body Dementia.

@dbdugger - Daniel Brittain Dugger

SARS-CoV-2 Proteins Interact with Alpha Synuclein and Induce Lewy Body-like Pathology In Vitro https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8949667/

SARS-CoV-2 Proteins Interact with Alpha Synuclein and Induce Lewy Body-like Pathology In Vitro Growing cases of patients reported have shown a potential relationship between (severe acute respiratory syndrome coronavirus 2) SARS-CoV-2 infection and Parkinson’s disease (PD). However, it is unclear whether there is a molecular link between ... ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

SARS-CoV-2 Spike Protein S1 Domain Accelerates α-Synuclein Phosphorylation and Aggregation in Cellular Models of Synucleinopathy https://pubmed.ncbi.nlm.nih.gov/37897633/

SARS-CoV-2 Spike Protein S1 Domain Accelerates α-Synuclein Phosphorylation and Aggregation in Cellular Models of Synucleinopathy - PubMed The 2019 novel coronavirus disease (COVID-19) is an infectious disease that began to spread globally since 2019. Some COVID-19 patients have neurological complications, such as olfactory disorders and movement disorders, which coincide with the symptoms of Parkinson's disease (PD). Increasing imagin … pubmed.ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

Here is how I knew the protein was operating mechanistically as HIV's Vpr. SARS-CoV-2 and the DNA damage response https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10768691/

SARS-CoV-2 and the DNA damage response The recent coronavirus disease 2019 (COVID-19) pandemic was caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). COVID-19 is characterized by respiratory distress, multiorgan dysfunction and, in some cases, death. The virus is also ... ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

"HIV-1 causes double-strand breaks as a result of binding of its VPR protein to chromatin [71]. Vpr expression also activates ATM and leads to the formation of repair foci."

@dbdugger - Daniel Brittain Dugger

HIV-1 Vpr protein impairs lysosome clearance causing SNCA/alpha-synuclein accumulation in neurons https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8354668/

HIV-1 Vpr protein impairs lysosome clearance causing SNCA/alpha-synuclein accumulation in neurons Despite the promising therapeutic effects of combinatory antiretroviral therapy (cART), 20% to 30% of HIV/AIDS patients living with long term infection still exhibit related cognitive and motor disorders. Clinical studies in HIV-infected patients revealed ... ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

Call me crazy, I would argue a chronic SARS-Cov-2 infection is as much of a neglected disease as ME/CFS as individuals have been deprived by dumbasses of forty years of evidenced based medicine to save their lives.

@dbdugger — Daniel Brittain Dugger

Posted - September 3, 2023 at 10:30 AM

Saved - September 3, 2023 at 11:30 AM

reSee.it AI Summary

Post-COVID cognitive deficits remain unknown. A chronic SARSCov2 infection shares similarities with HIV, depleting CD4 cells and affecting the brain. Studies implicate various cell types, including astrocytes, perivascular macrophages, choroid plexus, pericytes, and microglia. Cognitive decline, CD4 depletion, and creatine clearance reduction are observed. Endothelial damage and CD4 depletion are related. Vascular reactivity index correlates with lower nadir CD4 count and LDL cholesterol. Society's fate lies in the hands of those who ignore these connections.

@dbdugger - Daniel Brittain Dugger

"How post-COVID-19 cognitive deficits develop remains unknown." Can only be said by those who fail to read the work of others and draw parallels. Folks should be ashamed of themselves for their lack of intellectual curiosity.

@dbdugger - Daniel Brittain Dugger

Let me show you how incredibly simple it is explain the neurocognitive complications that accompany a chronic SARS-Cov-2 infection.

@dbdugger - Daniel Brittain Dugger

On September 28, 2020 the entire medical establishment and those in academia were alerted to the fact that a chronic SARS-Cov-2 infection shared the hallmark of a chronic HIV infection, depletion of the CD4 compartment.

@dbdugger - Daniel Brittain Dugger

The VERY next day, this paper was published. https://pubmed.ncbi.nlm.nih.gov/32990925/

@dbdugger - Daniel Brittain Dugger

"However, it did not take long to discover that the disease could also attack the brain directly, which resulted in long-term cognitive impairment."

@dbdugger - Daniel Brittain Dugger

Did we see any meaningful action to prevent our society being plagued by senility? Of course we did not.

@dbdugger - Daniel Brittain Dugger

The following appears within the Intake form that I created and is used to interview an individual, asking about specific deficits they may have. Basal Gangia Cerebral Cortex Medulla Oblongata Cerebellum Thalamus Hypothalamus Corpus Callosum

@dbdugger - Daniel Brittain Dugger

Where does it also exist? Within the paper detailing the findings of Dr. Daniel Chertow, which was published December, 2021. https://assets.researchsquare.com/files/rs-1139035/v1_covered.pdf?c=1640020576

@dbdugger - Daniel Brittain Dugger

While I do not believe his paper goes so far as to identify specific cell types that have been productively infected, others do. Such as this one, discussing astrocytes. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9335203/

In SARS-CoV-2, astrocytes are in it for the long haul ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

And this one, implicating perivascular macrophages and the choroid plexus. https://www.nature.com/articles/s41586-021-03710-0

@dbdugger - Daniel Brittain Dugger

And this one, demonstrating pericyte involvement. https://academic.oup.com/cardiovascres/article/118/15/3085/6609448

@dbdugger - Daniel Brittain Dugger

Finally, the cell type that took a back seat to "microclots," the microglia. https://www.frontiersin.org/articles/10.3389/fncel.2021.670298/full

Microglial Implications in SARS-CoV-2 Infection and COVID-19: Lessons From Viral RNA Neurotropism and Possible Relevance to Parkinson’s Disease Since December 2019, humankind has been experiencing a ravaging severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) outbreak, the second coronavirus pandemic in a decade after the Middle East respiratory syndrome coronavirus (MERS-CoV) disease in 2012. Infection with SARS-CoV-2 results in Coronavirus disease 2019 (COVID-19), which is responsible for over 2.13.1 million deaths worldwide. With the emergence of a second and a third wave of infection across the globe, and the rising record of multiple reinfections and relapses, SARS-CoV-2 infection shows no sign of abating. In addition, it is now evident that SARS-CoV-2 infection presents with neurological symptoms that include early hyposmia, ischemic stroke, meningitis, delirium and falls, even after viral clearance. This may suggest chronic or permanent changes to the neurons, glial cells, and/or brain vasculature in response to SARS-CoV-2 infection or COVID-19. Within the central nervous system (CNS), microglia act as the central housekeepers against altered homeostatic states, including during viral neurotropic infections. In this review, we highlight microglial responses to viral neuroinfections, especially those with a similar genetic composition and route of entry as SARS-CoV-2. As the primary sensor of viral infection in the CNS, we describe the pathogenic and neuroinvasive mechanisms of RNA viruses and SARS-CoV-2 vis-à-vis the microglial means of viral recognition. Responses of microglia which may culminate in viral clearance or immunopathology are also covered. Lastly, we further discuss the implication of SARS-CoV-2 CNS invasion on microglial plasticity and associated long-term neurodegeneration. As such, this review provides insight into some of the mechanisms by which microglia could contribute to the pathophysiology of post-COVID-19 neurological sequelae and disorders, including Parkinson’s disease, which could be pervasive in the coming years given the growing numbers of infected and re-infected individuals globally. frontiersin.org

@dbdugger - Daniel Brittain Dugger

Every single cell type that constitutes the Central Nervous System in HIV has been productively infected by SARS-Cov-2, with microglia serving as the primary cell type. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6821723/

@dbdugger - Daniel Brittain Dugger

While folk "elucidate" and "tease out" that which could be explained had they read, as I have done, individuals are experiencing a decline in their cognition, CD4 population, and creatine clearance levels.

@dbdugger - Daniel Brittain Dugger

What I find to be remarkable is so many folk bitch about endothelial damage and continue to ignore the depletion of the CD4 compartment, as if they are not related. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7268551/https://pbs.twimg.com/card_img/1696143174819807232/m2AAd_8_?format=jpg&name=small

Page not available - PMCTwitterFacebookLinkedInGitHubSM-TwitterSM-FacebookSM-Youtube ncbi.nlm.nih.gov

@dbdugger - Daniel Brittain Dugger

"Vascular reactivity index, marker of endothelial dysfunction, showed a significant correlation with lower nadir CD4 count (p = 0.003) as well as low-density lipoprotein cholesterol (p = 0.02)."

@dbdugger - Daniel Brittain Dugger

I've all but given up on those who were unfortunately placed in a position to determine the fate of our society. You probably should, too.

@dbdugger — Daniel Brittain Dugger

Posted - August 22, 2023 at 1:20 PM

Saved - August 22, 2023 at 6:30 PM

reSee.it AI Summary

The fight against the virus requires a new approach. Drawing from HIV medicine, we see the need for pharmaceutical interventions alongside vaccine development. Strategies like Post Exposure Prophylaxis, PreExposure Prophylaxis, and Treatment as Prevention have proven effective. To preserve immune competence and cognition, we must adopt Treatment as Prevention for chronic SARSCov2 infections. Durable suppression is crucial to prevent resistant strains. However, the lack of viral load tests hinders progress. Combination therapy is essential, targeting multiple points in the replication cycle. Let's repurpose possible candidates and prioritize reduction in viral load to ensure success. Antiviral deferral has dire consequences. We must act now.

@dbdugger - Daniel Brittain Dugger

No, we will not conquer the virus. Considering the fact that we have yet to borrow from 40 years of HIV medicine, one has to wonder if we really want to conquer the virus.

@dbdugger - Daniel Brittain Dugger

With SARS-Cov-2, it is quite easy to observe that which we have seen with HIV over the past 40 years. Viral evolution outpacing vaccine development. An aversion to rely upon nonpharmaceutical interventions, masks with SARS-Cov-2 and condoms with HIV.

@dbdugger - Daniel Brittain Dugger

With HIV medicine, the decision was made to pursue pharmaceutical interventions contemporaneously with vaccine development. First, came Post Exposure Prophylaxis.

@dbdugger - Daniel Brittain Dugger

The next innovation allowed for an individual to take their health into their own hands, to prevent the acquisition of HIV. It is referred to as Pre-Exposure Prophylaxis.

@dbdugger - Daniel Brittain Dugger

Finally, one of the most remarkable innovations, allows an individual living with HIV to prevent its transmission and burdening another individual with the condition. It is referred to as Treatment as Prevention.

@dbdugger - Daniel Brittain Dugger

With millions living with a chronic SARS-Cov-2 infection, it is quite clear that if we have any interest in preserving what is left of these individual's immune competence and cognition, we must go in reverse. Treatment as Prevention must be the strategy adopted.

@dbdugger - Daniel Brittain Dugger

We knew this was going to be necessary as soon as the first monoclonal was wiped out as it was suggestive of either viral persistence or too short of a duration of therapy.

@dbdugger - Daniel Brittain Dugger

Considering evidence of microglia involvement, we now know that durable suppression will be required for life so as to prevent the emergence of resistant strains through "CNS Escape."

@dbdugger - Daniel Brittain Dugger

Unfortunately, we are without the tools to allow us to even begin the process of implementing a Treatment as Prevention model. Namely, that of a viral load test.

@dbdugger - Daniel Brittain Dugger

It is through the use of a viral load test that those in HIV medicine were able to determine the target log copy that would not only prevent disease progression but forward transmission, as well.

@dbdugger - Daniel Brittain Dugger

As for your intimation that combination therapy will be required, it most certainly will. The use of what is described as a monotherapy invites resistance developing as a consequence of not targeting enough points in the replication cycle.

@dbdugger - Daniel Brittain Dugger

Additionally, the literature is quite clear as to what is required to arrest the cortical thinning, cortical atrophy, and begin the process of resolving frontal lobe hypometabolism. It is combination therapy.

@dbdugger - Daniel Brittain Dugger

Are there possible candidates that could be repurposed? It appears so. However, without the viral load test mentioned above, there isn't a way to appreciate a log copy reduction during the drug trials.

@dbdugger - Daniel Brittain Dugger

An inability to observe this reduction allows individuals to assume that the drug is not working, ignoring the fact that millions have been allowed to have their viral loads shoot through the roof as a consequence of antiviral deferral.