"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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Why women are more likely to develop long COVID?
This new preprint is fascinating - it’s the first to experimentally explain why women are more prone to long COVID, even though men more often end up hospitalized during acute infection🧵
Researchers infected male and female mice with SARS-CoV-2 (B.1.621) and tracked them for 3 months.
Males - worse acute illness, lung damage, higher mortality.
Females - milder acute phase, but later showed memory loss, brain inflammation, and activated microglia long after recovery.
The key difference wasn’t hormones - it was the X chromosome.
Two X chromosomes (XX) protect in the acute phase,
but make the immune system more likely to stay on afterwards.
One X (XY or X0) = worse acute COVID, fewer long-term effects.
Possibly one of the most important studies on EBV and human immunity in a long time.
It shows that a special type of immune cell - γδ T cells (Vδ1) - can detect and destroy EBV-infected cells even when the virus hides from the classical immune system.🧵
The team used a human blood infection model and single-cell RNA sequencing to map every immune response to EBV.
This unbiased approach revealed players that traditional assays often miss - including the elusive γδ T cells.
In healthy people, EBV control relies on teamwork
CD8 T cells and NK cells handle direct killing,
but γδ T cells (Vδ1) join the fight as a third, previously underappreciated line of defense.
A finally published study from the Children’s Long COVID Clinic in Los Angeles confirms that long COVID in children is real, multisystemic, and can persist for over a year.🧵
The study followed 123 children (ages 0–21, mean 13 yrs).
On average, symptoms began 5 weeks after infection.
Many improved within months - but some remained ill even after 18 months.
Most common symptoms:
fatigue (93%)
headache (70%)
exercise intolerance (53%)
dizziness (44%)
brain fog (41%)
muscle/joint pain (29%)
shortness of breath or abdominal pain (28%)
palpitations (26%)
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.
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.
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.