TruthArchive.ai - Tweets Saved By @ZdenekVrozina

@ZdenekVrozina - Zdenek Vrozina

Viruses like HIV and CMV don’t just evade immunity - they reshape the host from within. One way they do it? By targeting the cell’s ability to make proteins. SARS-CoV-2 belongs in this group. It interferes with how ribosomes are made and used. What that means - and why it matters 🧵

@ZdenekVrozina - Zdenek Vrozina

Viruses like HIV are known to: block protein translation rewire cell signaling change cellular behavior without altering DNA SARS-CoV-2 does the same. Its Nsp1 protein hijacks ribosomes - the core machinery that turns RNA into protein.

@ZdenekVrozina - Zdenek Vrozina

Ribosomes are molecular machines that translate genetic instructions (mRNA) into proteins. Without them, a cell can’t repair itself, send immune signals, respond to stress or survive infection.

@ZdenekVrozina - Zdenek Vrozina

SARS-CoV-2 hits ribosomes on two fronts: Nsp1 blocks existing ribosomes - shuts down translation Nsp1 blocks formation of new ones - interferes with rRNA processing in the nucleolus This causes both acute and lingering disruption of protein synthesis.

@ZdenekVrozina - Zdenek Vrozina

A 2024 study (Yerlici et al., Cell Reports) showed that Nsp1: enters the nucleolus binds to pre-rRNA prevents its processing and export So this stalls ribosome production - without needing to change the cell’s transcriptional program.

@ZdenekVrozina - Zdenek Vrozina

The result? A drop in protein-making capacity. The cell may survive, but it can’t make enough proteins to repair, signal, or defend itself. Homeostasis breaks down. Stress builds up. Regeneration falters. This can lead to: chronic fatigue inflammatory overload tissue repair failure immune exhaustion

@ZdenekVrozina - Zdenek Vrozina

And it gets deeper. Ribosomes shape gene expression. They’re not passive tools - they influence which mRNAs get translated, and when. So disrupting ribosome function selectively silences parts of the genome without touching the DNA.

@ZdenekVrozina - Zdenek Vrozina

A gene can be “on” - but if its mRNA doesn’t get translated, the protein never appears. This creates functional shutdown without any mutation or epigenetic change. It’s quiet, but powerful. The virus reprograms the cell by shifting what gets built - and what doesn’t.

@ZdenekVrozina - Zdenek Vrozina

More consequences of impaired ribosome function: misfolded proteins and ER stress faulty signaling proteins delayed cellular response to stress disrupted communication between organelles Systems begin to desynchronize - even without structural damage.

@ZdenekVrozina - Zdenek Vrozina

HIV behaves similarly: blocks translation of HLA and other key proteins reprograms epigenetic marks drives immune exhaustion and senescence CMV and EBV also alter host translation to favor their survival - at the host’s expense.

@ZdenekVrozina - Zdenek Vrozina

SARS-CoV-2 clearly fits this class. It’s not just an acute respiratory virus. It actively rewires protein synthesis - the core of how a cell adapts, regenerates, and defends itself. That leaves a lasting footprint on the body.

@ZdenekVrozina - Zdenek Vrozina

One consequence may be cancer risk: unbalanced translation of oncogenes impaired tumor suppressor pathways chronic stress and inflammation This creates a long-term environment that favors cellular transformation.

@ZdenekVrozina - Zdenek Vrozina

Ribosome disruption has system-wide effects - and they strongly resemble the profile of long COVID. That may not be a coincidence. If a virus throws off ribosomal balance, it can affect multiple organ systems at once.

@ZdenekVrozina - Zdenek Vrozina

Potential effects include: neuroinflammation, brain fog impaired blood cell regeneration muscle weakness, exercise intolerance temperature dysregulation autonomic dysfunction cellular senescence immune misfiring

@ZdenekVrozina - Zdenek Vrozina

What ties them together? A cell that can’t make the right proteins at the right time. Translation slows, stalls, or skews - and the system starts breaking down. No scar tissue, no visible damage - just dysfunction.

@ZdenekVrozina - Zdenek Vrozina

Long-term effects of SARS-CoV-2 may not stem from a single “injury.” They may result from disrupted control systems - like protein synthesis. Time, stress, and the body’s own compensations do the rest.

@ZdenekVrozina - Zdenek Vrozina

This mechanism isn’t brand new - but it’s been overlooked. It may help explain why some symptoms last for months after infection ends. And why they can affect so many systems at once.

@ZdenekVrozina - Zdenek Vrozina

Yerlici at al. 2024. SARS-CoV-2 targets ribosomal RNA biogenesis. https://www.cell.com/cell-reports/fulltext/S2211-1247(24)00219-5?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS2211124724002195%3Fshowall%3Dtrue

@ZdenekVrozina - Zdenek Vrozina

@tryna_do_rite Yes, I do wear N95 in all shared indoor air.

@ZdenekVrozina - Zdenek Vrozina

@AnneTakeuchi I understand the connotations. I think what really matters is how we talk about it. Let’s focus on the mechanisms - and use them to show that experience from the past teaches us to be cautious today.

@ZdenekVrozina - Zdenek Vrozina

SARS-CoV-2 isn’t HIV. We’re talking about similar mechanisms. Good news: ribosomes are regularly renewed in healthy cells. But if stem cells are damaged or epigenetically reprogrammed, regeneration may be slow, incomplete, or blocked. The full scope of downstream effects is still unfolding.

@ZdenekVrozina - Zdenek Vrozina

@biologists1 Yerlici doesn’t discuss viral translation directly. Others showed SARS-CoV-2 bypasses Nsp1 translational shutoff via the SL1 in its 5′ UTR. No IRES confirmed yet.

@ZdenekVrozina - Zdenek Vrozina

@k3burch I’m so sorry to hear that. Many are now dealing with persistent post-viral illness triggered by this double hit.

@ZdenekVrozina - Zdenek Vrozina

@Zobbie137 The mRNA vacc is a passive template. It uses ribosomes like a copy machine only. It contains no active proteins or sequences that enter the nucleus, modify ribosomes, or interfere with their production.

@ZdenekVrozina - Zdenek Vrozina

@Krta1972 No, this isn’t a supply problem - it’s a machinery problem.

@ZdenekVrozina - Zdenek Vrozina

How COVID-19 Might Be Accelerating HPV-Related Cancer - with lessons from HIV🧵

@ZdenekVrozina - Zdenek Vrozina

COVID-19 isn’t just a lung infection. A new study of over 1.2 million women found something alarming - women who had COVID later developed more HPV-linked cancers. Cervical cancer risk up 67%, anal 92%, vulvar 98%, oropharyngeal 78%.

@ZdenekVrozina - Zdenek Vrozina

A real case shows how fast it can happen. One woman had a precancerous lesion on her cervix (CIN2). Normally, these take years to evolve. After COVID? It turned into early cancer in just 3 months. The virus wasn’t in her cervix. The culprit? Her immune system was wrecked - T cells & NK cells had collapsed. https://pubmed.ncbi.nlm.nih.gov/36399874/?

COVID-19 can lead to rapid progression of cervical intraepithelial neoplasia by dysregulating the immune system: A hypothesis - PubMed COVID-19 is a multisystem disease and cause of a global pandemic. Lately, cases of disease progression of HPV-infected CIN under SARS-CoV-2 infection were reported giving rise to the hypothesis of direct virus-infection induced pro-carcinogenic effect of SARS-CoV-2. We herein present a case of rapid … pubmed.ncbi.nlm.nih.gov

@ZdenekVrozina - Zdenek Vrozina

We’ve seen this movie before. HIV makes HPV-driven cancers skyrocket. Anal cancer up to 80× more common in HIV+ people. Why? HIV knocks down the immune guardrails - and, crucially, some of its proteins directly push cells toward malignancy. https://pmc.ncbi.nlm.nih.gov/articles/PMC7689909/

A meta‐analysis of anal cancer incidence by risk group: Toward a unified anal cancer risk scale Certain population groups are known to have higher than average anal cancer risk, namely persons living with HIV (PLHIV), men who have sex with men (MSM), women diagnosed with human papillomavirus (HPV)‐related gynecological precancerous lesions or ... pmc.ncbi.nlm.nih.gov

@ZdenekVrozina - Zdenek Vrozina

Meet Tat & gp120 - HIV’s cancer accomplices. They trigger EMT - cells lose their brick wall epithelial shape, turn flexible & invasive. In lab tests, invasiveness jumped 2–3×. Tat even boosts HPV’s E6, which shreds p53 - the cell’s genome guardian. Result? HPV + HIV = a perfect storm. https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2025.1541532/full

Frontiers | HIV-1 Tat-induced disruption of epithelial junctions and epithelial-mesenchymal transition of oral and genital epithelial cells lead to increased invasiveness of neoplastic cells and the spread of herpes simplex virus and cytomegalovirus Human immunodeficiency virus (HIV-1) transactivator Tat is a unique multi-functional viral protein secreted by infected cells. Although its primary function ... frontiersin.org

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Now here’s the twist - SARS-CoV-2 seems to have similar tricks. Spike protein alone can push cells into EMT, activating Snail, the master switch of invasion. In mice, that meant more metastasis. That’s eerily close to what gp120/Tat do. https://pmc.ncbi.nlm.nih.gov/articles/PMC8167694/

Epithelial-mesenchymal transition induced by SARS-CoV-2 required transcriptional upregulation of Snail The engagement of human angiotensin-converting enzyme 2 (hACE2) and SARS-CoV-2 spike protein facilitate virus spread. Thus far, ACE2 and TMPRSS2 expression is correlated with the epithelial-mesenchymal transition (EMT) gene signature in lung cancer. ... pmc.ncbi.nlm.nih.gov

@ZdenekVrozina - Zdenek Vrozina

Spike vs p53? Spike meddles with p53 too. Study found spike stabilized p53 - but then silenced its voice. p53 couldn’t turn on repair genes (like p21). The cell’s safety brake was there - but disconnected. In vitro. https://www.oncotarget.com/article/28582/text/

Transfected SARS-CoV-2 spike DNA for mammalian cell expression inhibits p53 activation of p21(WAF1), TRAIL Death Receptor DR5 and MDM2 proteins in cancer... | Oncotarget https://doi.org/10.18632/oncotarget.28582 Shengliang Zhang, Wafik S. El-Deiry oncotarget.com

@ZdenekVrozina - Zdenek Vrozina

Don’t forget the immune angle. Severe COVID burns out T cells, ramps up PD-1/PD-L1. That’s the same escape hatch HPV cancers use to hide. HPV cancers also exploit PD-L1. COVID may widen that escape hatch. https://www.mdpi.com/2077-0383/12/10/3539

@ZdenekVrozina - Zdenek Vrozina

Put it together. COVID could be an accelerant EMT + invasion (like HIV), p53 silencing, exhausted immunity. All paths lead to one outcome - HPV lesions progressing faster into cancer.

@ZdenekVrozina - Zdenek Vrozina

What’s next? Expose HPV+ cells to SARS-CoV-2 proteins, measure EMT/E6/p53. Use HPV-transgenic mice to test synergy. Compare tissues from patients with/without prior COVID for PD-L1, IL-6, exhausted T cells. If confirmed, this synergy could change how we screen & protect HPV+ patients post-COVID.

@ZdenekVrozina - Zdenek Vrozina

We ignored the lessons from HIV. It showed us how a virus can quietly amplify another’s cancer potential. COVID may be repeating that script - and we can’t afford a sequel.

@ZdenekVrozina - Zdenek Vrozina

And that’s just the first cancer type where we already have hard data. Given how SARS-CoV-2 disrupts p53, fuels EMT, and exhausts T-cells, it may not stop at HPV-driven cancers. The spectrum could be much wider.

@ZdenekVrozina - Zdenek Vrozina

The second big group are hepatocellular carcinomas (HBV/HCV). And beyond them, EBV, HHV-8, HTLV-1 each drive their own malignancies. If COVID weakens immune control, the real question is - which ones will it speed up? @dbdugger

@ZdenekVrozina - Zdenek Vrozina

@dbdugger Shih at al., SARS-CoV-2 infection heightens the risk of developing HPV-related carcinoma in situ and cancer. Discover oncology. https://link.springer.com/article/10.1007/s12672-025-03403-4

SARS-CoV-2 infection heightens the risk of developing HPV-related carcinoma in situ and cancer - Discover Oncology This study aims to investigate the impact of SARS-CoV-2 infection on HPV-related cancer and carcinoma in situ. We utilized data from TriNetX, a database en link.springer.com

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Prenatal COVID and Infant Brain Development - New Data, Alarming Trends We begin with a 2025 study from Brazil, the first to directly link cytokines in cord blood with neurodevelopmental delays in toddlers exposed to SARS-CoV-2 in the womb. https://www.nature.com/articles/s41390-025-04192-w

Cord blood cytokines/chemokines linked to delays in toddlers exposed to SARS-CoV-2 prenatally - Pediatric Research Maternal infections are linked to neurodevelopmental impairments, highlighting the need to investigate SARS-CoV-2-induced immune activation. This study aimed to evaluate the impact of maternal infection on neurodevelopment and investigate whether cytokine and chemokine profiles predict delays at 24 months. Conducted in Brazil (January 2021–March 2022), this follow-up study included 18 SARS-CoV-2 positive pregnant women at 35–37 weeks’ gestation, 15 umbilical cord blood samples, and blood samples from 15 children at 6 months and 14 at 24 months. Developmental delay was defined using the Bayley Scales of Infant and Toddler Development, Third Edition, with scores below 90 in cognitive, communication, or motor domains. At 6 months, 33.3% of infants exhibited cognitive delays, 20% communication delays, and 40% motor delays, increasing to 35.71%, 64.29%, and 57.14% at 24 months, respectively. Elevated interferon-gamma and tumor necrosis factor-alpha in cord blood correlated with cognitive delays, while interleukin (IL)-6, IL-8, IL-17, and IL-1β were associated with motor delays. Increased C-X-C motif chemokine ligand 10 and other cytokines were associated with communication delays. Maternal SARS-CoV-2 may impact infant neurodevelopment, as early cytokine elevations correlate with delays, highlighting the importance of early monitoring and interventions to reduce long-term effects. nature.com

@ZdenekVrozina - Zdenek Vrozina

At 24 months of age: 36% showed cognitive delays 64% had language delays (sic) 57% had motor delays And here’s the striking part: these delays were predicted by the cytokine profile in umbilical cord blood.

@ZdenekVrozina - Zdenek Vrozina

Elevated inflammation markers: IFN-γ & TNF-α - cognitive delays IL-6, IL-8, IL-17, IL-1β - motor delays CXCL10 - language delays This is strong evidence for maternal immune activation - a mechanism also seen in autism and schizophrenia research.

@ZdenekVrozina - Zdenek Vrozina

A UCLA study tracked 211 COVID-exposed children. At 28 months, 11% screened positive for autism spectrum disorder - far above the expected 1-2%. Some had activated microglia and neuroinflammatory markers in blood at birth. https://www.japantimes.co.jp/news/2024/12/27/world/science-health/covid-pregnancy-autism-study/

COVID pregnancies may have boosted autism risk, study shows 'There’s something really going on,” pediatric infectious diseases physician Karin Nielsen says. 'We don’t want to alarm the world, but that’s what our data are showing.” japantimes.co.jp

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Then comes the placenta. A Michigan pathology review identified SARS-CoV-2 placentitis even in asymptomatic mothers (2025): fibrin deposition intervillositis trophoblast necrosis confirmed virus in placental tissue Risk: fetal hypoxia, IUGR, stillbirth https://meridian.allenpress.com/aplm/article/doi/10.5858/arpa.2024-0247-RA/506106/SARS-CoV-2-Placentitis-A-Review-of-Pathologic

@ZdenekVrozina - Zdenek Vrozina

Structural brain changes have also been observed. An Italian study found ultrasound abnormalities in 23% of newborns exposed to SARS-CoV-2 in utero - vs. 16% of controls. Most were minor (cysts) - but statistically significant. https://ijponline.biomedcentral.com/articles/10.1186/s13052-024-01826-3

Cranial ultrasonographic findings in newborns exposed to SARS-CoV-2: a single-centre cross-sectional analysis - Italian Journal of Pediatrics SARS-CoV-2’s potential consequences on the developing brain are still unknown. The aim of this study was to describe cranial ultrasonographic (cUS) findings in a population of newborns exposed to SARS-CoV-2 born at San Marco Hospital in Catania. Two cohort of newborns, one exposed to SARS-CoV-2 both during gestation and at birth and one unexposed, were enrolled in this cross-sectional study conducted according to the STROBE guidelines (Strenghtening the Reporting of Observational Studies in Epidemiology) and underwent cUS. We performed a statistical analysis using the Fisher’s exact test to assess whether significant differences among the two groups existed. we enrolled 139 exposed newborns (62 females, 77 males with median gestational age 38.4 ± 1.9 W and median weight at birth 3142.8 ± 594.4 g) and 139 unexposed newborns (60 females, 79 males with median gestational age 38,9 ± 1.3 W and median weight at birth 3230 ± 336 g). cUS abnormalities were found in 32 exposed patients (23%) and in 23 (16.5%) unexposed patients. A statistically significant difference was found in the incidence of minor intracranial abnormalities (p 0.036) between exposed and unexposed patients and between newborns exposed during pregnancy and unexposed patients (p 0.016). in our experience, the incidence of minor intracranial abnormalities was higher in SARS-COV-2-exposed newborns. Our results must be taken with caution and need further confirmation in larger studies but suggest to consider performing cUS at birth in newborns exposed to SARS-CoV-2 in research contexts. ijponline.biomedcentral.com

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Harvard researchers found the effect is sex-specific. Boys born to SARS-CoV-2 positive mothers had 2× the risk of neurodevelopmental diagnoses at 12 months. Girls showed no such increase. https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2802745

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And finally: epigenetics. A Swedish 2025 study showed that even mild maternal COVID-19 alters DNA methylation in the infant’s immune and brain-related genes. Genes involved in neuron signaling, interferon response, and neurodevelopment were affected. https://www.medrxiv.org/content/10.1101/2025.05.10.25327356v1

DNA methylation changes in infants of mothers with SARS-CoV-2 infection during pregnancy medRxiv - The Preprint Server for Health Sciences medrxiv.org

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In summary: SARS-CoV-2 exposure in utero can leave a long shadow - through neuroinflammation placental dysfunction brain structure changes and epigenetic rewiring The science is clear. The risks are real.

@ZdenekVrozina - Zdenek Vrozina

But this isn’t just a warning. It’s a call to action. Expectant parents deserve clear, science-based information on prenatal COVID risks. No child should suffer lifelong harm from an exposure their mother wasn’t told mattered. We are losing futures before they’re even born.

@ZdenekVrozina - Zdenek Vrozina

After five years of research, dozens of peer-reviewed studies, and signals from across continents…how is it possible that public health remains silent? No warnings. No prenatal screening protocols. No public campaigns. No plan. The children deserved better. And still do. @szupraha @ZdravkoOnline