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.
Meanwhile, protective lipids drop.
Palmitoleate (anti-inflammatory lipokine)
Cerotate (peroxisomal function)
Squalene (antioxidant, skin barrier)
Loss of these defenses = more oxidative damage, weaker membranes, slower recovery.
The result is a shift
from anti-inflammatory to pro-inflammatory lipids, from cellular balance to lipid toxicity.
Mechanistically, this mirrors what phospholipase toxins do - break membranes and trigger inflammation.
SARS-CoV-2 gains an advantage by doing this
hijacks host lipids for replication,
weakens structural barriers,
amplifies inflammation,
leaves behind long-lasting metabolic scars.
So the toxin-like label isn’t a strong metaphor.
It’s a biochemical reality
metabolic rewiring - lipid peroxidation - cellular injury.
Same principle as toxins - different origin.
The virus doesn’t carry a toxin.
It makes us produce it.
From our own fatty acids, enzymes, and membranes.
That’s the quiet genius - and the danger - of SARS-CoV-2.
Soler-Jiménez et al., Solid-phase microextraction of sweat components of patients positive for SARS-CoV-2 for identification of possible biomarkers. nature.com/articles/s4159…
Interestingly, the same toxin-like signature appears in snakebite victims.
↑ Palmitic acids
↓ squalene
↑ lipid oxidation
The sweat chemistry looks similar.
The difference?
A snake injects the toxin.
SARS-CoV-2 makes your own cells produce it from within.
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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%)
"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 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.