Zdenek Vrozina Profile picture
Oct 14 14 tweets 2 min read Read on X
"The statement that SARS-CoV-2 is airborne AIDS may be an oversimplification, but it draws attention to emerging evidence showing that the virus induces a distinct form of acquired immunodeficiency (AID)."
A new paper in AJPM Focus (Elsevier, 2025)🧵
Science is beginning to recognize the true severity of SARS-CoV-2’s long-term impact. A new paper in AJPM Focus carries a striking title:
“COVID-19 is Airborne AIDS: provocative oversimplification, emerging science, or something in between?”
The authors (Salamon, Pretorius, Ewing, Bar-Yam, and others) review a large body of evidence.
Their conclusion - SARS-CoV-2 is not HIV - but it shares key biological traits with it -
immune exhaustion, viral persistence, and systemic inflammation.
COVID-19 can cause deep immune dysfunction -
reduced and exhausted T and B cells, loss of NK cells, endothelial injury, and microclots that starve tissues of oxygen.
These effects can persist and accumulate with reinfections.
Unlike HIV, SARS-CoV-2 spreads through the air, infects repeatedly, and leaves a cumulative immune toll on the population.
Reinfections are not harmless - they may compound immune and neurological damage over time.
The neurological parallels are striking.
Long COVID (SAND) resembles HIV-related cognitive decline (HAND).
Both involve neuroinflammation, brain hypometabolism, and measurable cognitive loss - memory, focus, even IQ.
Both viruses accelerate biological aging - epigenetically, mitochondrial, and immunological.
HIV does so slowly. SARS-CoV-2 can trigger it within months.
The paper’s key message -
COVID-19 is not AIDS, but it represents a form of acquired immune dysfunction.
A blunt but necessary statement - one that forces us to face the chronic nature of this virus.
The phrase Airborne AIDS is provocative - but it’s meant as a warning, not an exaggeration.
It reflects growing evidence that SARS-CoV-2 can reshape the immune system at a population level.
The authors call for -
Research into viral persistence and immune biomarkers
Long-term care for those affected
And renewed focus on airborne prevention - because transmission is still ongoing.
The pandemic didn’t end.
Only the narrative did.
Biologically, it continues - and science is finally catching up to that truth.
Spela Salamon at al., COVID-19 is “Airborne AIDS”: provocative oversimplification, emerging science, or something in between? @SalamonSMD @resiapretorius @yaneerbaryam @ArneauxK @DALupton @AndrewEwing11 ajpmfocus.org/article/S2773-…
To Public Health
Five years of inaction have exposed a systemic failure of purpose.
You were created to protect populations from harm - yet you looked away as evidence mounted of chronic, disabling disease. @szupraha @ZdravkoOnline @adamvojtech86
It’s time to reclaim the mission of public health.
To tell the truth, to prevent exposure, and to protect those already harmed.
History will not forgive silence when the science was clear.

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More from @ZdenekVrozina

Oct 14
SARS-CoV-2 doesn’t produce a classic toxin.
But it reprograms our lipid metabolism so deeply that the cell enters a toxic, pro-inflammatory, oxidative state.
Functionally, it behaves like a toxin-like infection🧵
A new study analyzed sweat from 426 people using GC-MS.
The lipid profile alone could distinguish COVID+ from COVID− with >80% accuracy.
But what they found looks eerily similar to systemic envenoming - just without a snake.
In COVID+ individuals, two lipids rise sharply.
Palmitic acid + oleic acid
These lipids -
stabilize the spike protein (via palmitoylation),
activate inflammasomes,
disrupt mitochondria.
They create the biochemical foundation of a toxic state.
Read 10 tweets
Oct 13
COVID-19 doesn’t just cause inflammation.
It switches off the genes that repair blood vessels - and switches on those that drive inflammation and destruction.
And what’s worse - this state lasts for at least six months, long after the infection is gone🧵
Researchers studied endothelial progenitor cells - the special cells that normally repair blood vessels after injury.
In people recovering from severe COVID (before vaccines even existed), they found these repair cells were genetically reprogrammed.
The healing genes were switched off.
NOS3 - produces nitric oxide to relax vessels
KLF2 - master regulator of endothelial health
ANGPT1, TGFB1, SMAD6 - maintain vessel stability and repair
The body’s vascular repair system went silent.
Read 12 tweets
Oct 11
New preprint from Harvard & Massachusetts General Hospital -children with Long COVID show markedly increased levels of fibrinaloid microclots in their blood!
The highest levels appear in those with persistent SARS-CoV-2 spike protein in circulation🧵
Long COVID affects roughly 1 in 5 children after SARS-CoV-2 infection.
Common symptoms include fatigue, brain fog, pain, and shortness of breath.
Diagnosis remains largely clinical - we still lack objective lab biomarkers for pediatric LC.
To address this, the team led by Daniel Irimia and David Walt developed a microfluidic device that can quantifyfibrinaloid microclots - tiny, fibrin-like clots resistant to normal breakdown (fibrinolysis).
These structures can obstruct microcirculation and reduce tissue oxygen delivery.
Read 24 tweets
Oct 11
The study, conducted in a mouse model, shows that SARS-CoV-2 infection can alter epigenetic information in sperm - specifically the profile of small noncoding RNAs passed on at fertilization - and that these changes can be transmitted to the offspring🧵
These changes may influence the development of the nervous system and the stress response of the offspring, independently of the DNA sequence itself.
Male mice infected with SARS-CoV-2 were mated with uninfected females four weeks after recovery.
Their offspring showed no signs of infection, but exhibited changes in behavior and gene expression.
Read 11 tweets
Oct 10
COVID didn’t end - it changed the baseline of how often people fall ill, miss work, and drop out of the labor force. A new JAMA study shows the US now lives in a permanent flu-season mode, all year round🧵
COVID-19 has created a new year-round baseline of illness - its effects persist even without major waves or restrictions, pointing to chronic impacts from ongoing infection or post-infectious conditions, including long COVID.
This new health environment means lower productivity and a greater need for worker protections such as paid sick leave, improved ventilation, and infection prevention at workplaces.
Read 12 tweets
Oct 10
Post-COVID depression isn’t weakness.
It’s biology.
A landmark, important study shows how the virus leaves a measurable molecular trace - in the very proteins that protect your brain from degeneration🧵
A new study in Translational Psychiatry shows that psychiatric symptoms after COVID-19 aren’t just psychological.
They have a biological signature - measurable changes in blood proteins linked to the brain, metabolism, and immunity.
People who developed new depression, anxiety, PTSD, or insomnia after COVID showed distinct biochemical profiles compared to those who recovered fully or had other long COVID symptoms.
It’s not psychology.
It’s neurobiology.
Read 16 tweets

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