A possible new diagnostic approach to Long COVID.
Long COVID may involve microcirculatory blockages - tiny, persistent clots known as fibrinaloid microclots.
These abnormal fibrin structures resist breakdown and can obstruct blood flow in the smallest vessels.🧵
The result - local hypoxia, fatigue, muscle weakness, brain fog - classic long COVID symptoms.
Even a slight obstruction means tissues aren’t getting enough oxygen.
A new preprint study by Kell & Pretorius proposes a non-invasive diagnostic tool -
thermal imaging (IR thermography) - using skin temperature patterns to visualize microcirculatory dysfunction.
Cooler areas = reduced blood flow (microcirculatory deficit).
Warmer areas - may show inflammation or compensatory hyperperfusion.
Together, they form a thermal fingerprint of endothelial dysfunction.
Why it matters.
Low-cost (even smartphone-compatible), non-invasive, repeatable, useful for tracking recovery or therapy response
The authors note that thermal imaging could be combined with other biomarkers of inflammation and coagulation to provide a more complete picture of vascular health.
“Before thermal imaging can be widely adopted in the clinic, there is a need for careful protocol standardisation and calibration, along with the creation of large reference datasets to define what constitutes ‘normal’ perfusion.”
Interpretation matters.
Temperature alone doesn’t directly reflect microcirculation - it must be read in context.
They recommend combining IR imaging with
nailfold capillaroscopy
laser speckle or Doppler analysis
biomarkers of endothelial dysfunction (eg von Willebrand factor)
Together, these offer both quantitative and visual insight into microvascular integrity.
Sum:
Thermal imaging can make the invisible visible - revealing microcirculatory blockages in Long COVID as a real fingerprint of endothelial dysfunction and impaired tissue perfusion.
This study by Kell & Pretorius is not focused specifically on Long COVID - it explores thermal imaging as a general tool to assess microcirculatory health across many conditions (diabetes, sepsis, vascular disease, etc).
The link to Long COVID is contextual, since fibrinaloid microclots and endothelial dysfunction are shared features across these disorders.
D. Kell, E. Pretorius, Assessing the Health and Functionality of the Microcirculation Using Thermal Imaging. preprints.org/manuscript/202…
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Smell loss after COVID isn’t just a sensory symptom.
It’s a window into how the virus reshapes the emotional brain.
New imaging data reveal microstructural changes in the amygdala - linking smell, mood, and neuroplastic stress🧵
A new MRI study found structural changes in the amygdala - the brain’s emotional hub - in people with long term smell loss after COVID-19.
This goes far beyond the nose.
Loss of smell after COVID isn’t just damage to nasal cells.
In some people it persists for months or years - and the brain adapts.
Researchers used diffusion tensor MRI (DTI) to examine microstructural white-matter changes in key olfactory–emotional regions.
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.
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.