Zdenek Vrozina Profile picture
Health Care Consulting
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Nov 3 19 tweets 3 min read
A experimental study in Scientific Reports shows that the SARS-CoV-2 spike protein alone can trigger an autoimmune response against the ACE2 receptor - the very receptor the virus uses to enter cells.
The mechanism mirrors tissue damage seen in severe COVID-19🧵 This study is a proof-of-concept.
When the immune system reacts to the SARS-CoV-2 spike protein, part of that response can flip into autoimmunity against ACE2, the receptor the virus normally uses to enter cells.
Nov 3 13 tweets 3 min read
A massive Swedish study on Nature Communications Medicine tracked 810,851 people after COVID.
Only 1.4% received an official post-COVID-19 condition (PCC) diagnosis - but that reflects only those who made it into the system.
Real prevalence of long COVID is many times higher🧵 Who was most likely to be diagnosed with PCC?
severe acute infection
unvaccinated status
female sex, older age
higher education, essential jobs (healthcare, teachers, drivers…)
pre-existing conditions - asthma, thrombosis, fibromyalgia, depression, anxiety, stress disorders
Nov 2 10 tweets 2 min read
While COVID-19 (Omicron) in children is often called mild, new evidence shows a darker side.
For a small fraction who develop brain inflammation, it becomes a deadly and disabling lottery.
The Lottery of Consequences🧵 A new multicenter study in Pediatric Neurology followed 102 children with COVID-19 related encephalopathy or encephalitis.
The outcome?
Half of them either died or were left severely disabled.
Nov 1 12 tweets 2 min read
A new paper in Pathogens makes a bold claim:
Aging, HIV, and Long COVID - three very different conditions - might share a common root cause - mitochondrial dysfunction.
Different paths, same destination🧵 The authors see mitochondria not as cellular batteries only, but as conductors of life.
When their rhythm falters, the whole orchestra follows - energy drops, immunity weakens, repair fails.
That’s the hidden thread connecting aging, HIV, and Long COVID.
Oct 31 14 tweets 3 min read
New study in Journal of Neuroinflammation, 2025, reveals how the SARS-CoV-2 spike protein alone - without the whole virus - can trigger inflammation and cellular aging in human brain cells - astrocytes.
The key - activation of the innate immune receptor TLR7.🧵 The spike’s S1 subunit enters astrocytes and accumulates in endolysosomes - the cell’s recycling centers.
Inside, it causes loss of acidity, membrane damage, and enzyme leakage (galectin-3, cathepsin B).
Result - inflammatory signaling and cellular senescence begin.
Oct 31 14 tweets 2 min read
Another study adds to growing evidence:
Children exposed in utero to maternal COVID-19 face a higher risk of neurodevelopmental issues by age 3.
It’s part of a broader pattern showing how SARS-CoV-2 can leave long biological traces - even before birth🧵 Study in Obstetrics & Gynecology, 2025
18,124 births (Mass General Brigham, 2020-2021).
861 mothers had confirmed SARS-CoV-2 infection during pregnancy.
By age 3, 16.3% of exposed children had a neurodevelopmental diagnosis vs 9.7% of unexposed.
Oct 28 5 tweets 1 min read
MRI alone may not be enough to rule out post-COVID heart inflammation.
A new JACC 2025 study found that even young, previously healthy adults with normal ECG, echo, and MRI can have microscopic heart damage - inflammation, microvascular damage, and cell necrosis.🧵 The study evaluated 423 long-COVID patients with persistent chest pain.
Most had normal or near-normal cardiac MRI, with only subtle changes in strain or perfusion.
Oct 27 24 tweets 4 min read
A new Russian review in IJMS shows how SARS-CoV-2 reshapes the epigenome - weaving together known mechanisms into something deeper.
It’s not just long COVID.
It’s a virus that rewrites the factory that makes immune cells - the bone marrow🧵 Zolotarenko puts special emphasis on this point.
The changes don’t appear in mature immune cells -
they start in their progenitors.
These hematopoietic precursors are born misprogrammed inside the marrow.
Oct 25 17 tweets 3 min read
A new important study in Frontiers in Immunology shows that repeated SARS-CoV-2 infections are beginning to display the same patterns seen in chronic viral infections - narrowing of the T-cell repertoire, exhaustion, and loss of immune flexibility (!)🧵 The immune repertoire doesn’t fully recover after infection. Diversity shrinks, and with reinfection the system no longer returns to balance.
Oct 24 9 tweets 2 min read
A study from Krakow followed hospitalized COVID-19 patients for five years to see if their initial immune profiles - T, B, and NK cells - could predict who would
die in the following years, or develop long COVID.🧵 Out of 103 patients from 2020, researchers followed 80 over 54 months.
23 had died, 57 were alive - and about half of those survivors (29 people) still lived with long COVID symptoms.
That’s one of the longest immune follow-ups after COVID-19 so far.
Oct 23 19 tweets 3 min read
A new preprint from Aarhus University shows something striking:
people with post-COVID, MCS, and functional disorders all share the same brain pattern -
split hemispheres, weakened bridges between left and right (!),
overloaded smell and sensory circuits🧵 The study scanned 57 women (post-COVID, MCS, FSD, controls) using diffusion MRI (DTI).
It didn’t measure brain activity, but rather its wiring - the white-matter highways that carry information between regions.
Oct 22 18 tweets 3 min read
A new study strengthens the view that SARS-CoV-2:
disrupts brain homeostasis,
alters ionic & neurotransmitter balance,
and triggers lasting epigenetic reprogramming.
Researchers exposed human primary astrocytes to Delta and Omicron.
The results are striking🧵 Astrocytes were infected with Delta and Omicron at a very low viral load (MOI 0.2).
After just 6 hours, RNA-seq revealed major transcriptional shifts
Omicron deregulated 346 genes (197 ↑, 149 ↓)
Delta deregulated 341 (215 ↑, 126 ↓)
About half of the changes overlapped.
Even minimal exposure triggered broad molecular changes within hours.
Oct 22 13 tweets 3 min read
Even though Omicron often causes milder illness, it leaves a clear metabolic footprint disrupting liver, immune, and energy metabolism.
A new study shows that even 2-4 weeks after recovery, the body does not return to normal metabolic state🧵 Researchers analyzed blood serum from 300 Omicron patients, 200 recovered, and 380 healthy controls.
Using LC-MS metabolomics, they tracked hundreds of molecules revealing how the infection affects the liver, mitochondria, and immune system.
Oct 21 11 tweets 2 min read
For the first time ever, a human body was instructed to make lab-designed antibodies against SARS-CoV-2 - by itself - from synthetic DNA.
One shot.
No virus.
Protection lasting over a year.🧵 A new Nature Medicine study tested something called DNA-encoded monoclonal antibodies (DMAbs).
Instead of injecting ready made antibodies, scientists injected synthetic DNA that tells your cells how to make them.
Your muscle becomes a mini factory for antibodies.
Oct 20 22 tweets 4 min read
SARS-CoV-2 is not just a respiratory virus. It acts more like an epigenetic manipulator - a virus that rewires how our genes are read and expressed. A new study shows how the virus edits the body’s epigenetic code🧵 Instead of simply damaging cells, it reprograms the host’s immune system, changing the molecular instructions that guide how the body responds to infection.
Oct 18 16 tweets 3 min read
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.
Oct 17 11 tweets 2 min read
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.
Oct 15 17 tweets 3 min read
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.
Oct 15 11 tweets 2 min read
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.
Oct 15 11 tweets 2 min read
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.
Oct 14 14 tweets 2 min read
"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?”