Zdenek Vrozina Profile picture
Oct 24 9 tweets 2 min read Read on X
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.
During the acute infection, those with severe disease showed a collapse of T and NK cells.
Their total T cells dropped to a median of 340 per µl (vs 705 in milder cases).
CD4+ helper T cells fell to 183 vs 452, and CD8+ cytotoxic T cells to 109 vs 227.
Even NK cells were lower (107 vs 157).
Meanwhile, the proportion of B cells was paradoxically higher - 18.5% vs 12.5%.
This imbalance wasn’t just a marker of severity - it predicted who would live or die.
Those who eventually died already had about 40–50% lower T and NK cell counts during the infection.
At the same time, they had more B cells (19% vs 13%).
In short - the weaker the T/NK response at the start, the higher the chance of dying later.
And what about long COVID?
Half of the survivors reported symptoms like fatigue, brain fog, breathlessness, or joint pain -
but their initial immune profiles looked the same as those who recovered fully.
No differences in T, B, or NK cell levels at the time of infection.
So
Low T/NK cells predicted death,
but not long COVID.
That’s the key message.
COVID-19 left behind two distinct immune legacies:
Immune collapse - when the body’s defenses never fully recover, leaving long-term vulnerability and higher mortality.
Immune persistence - when the immune system keeps reacting to lingering viral antigens, driving long COVID.
Two very different post-viral paths.
One loses strength, the other balance.
The study didn’t specify what the patients died from or how old they were at death.
At baseline, severe cases were older (63 y vs 59.5 y), but causes of late mortality weren’t analyzed.
Still - the signal is unmistakable.
Immune collapse predicted death long before medicine knew why.
Sometimes the immune system tells the story before medicine does.
Matyja-Bednarczyk at al., Baseline Dysregulation in B, T, and NK Cells in COVID-19 Predicts Increased Late Mortality but Not Long-COVID Symptoms: Results from a Single-Center Observational Study. mdpi.com/1999-4915/17/1…

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More from @ZdenekVrozina

Oct 25
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.
The study analyzed T-cell receptors in people after a first infection and after reinfection with SARS-CoV-2.
The result?
Reinfection isn’t just another infection - it leaves a measurable imprint on the immune system.
Read 17 tweets
Oct 23
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.
Result.
Interhemispheric connectivity - the bridge between left and right hemispheres - was reduced by 70% in all three patient groups.
That means information flow across the brain is slower, less coordinated, and less efficient.
Read 19 tweets
Oct 22
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.
Viral sensing and immune response.
Astrocytes primarily activated TLR2, but not RIG-I or NLRP3 - meaning they sensed the virus without launching a full antiviral storm.
Only 16 genes involved in interferon and interleukin signaling were affected.
Read 18 tweets
Oct 22
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.
Over 100 metabolites were significantly altered during infection - that’s expected in any acute illness.
What’s not expected?
Most of these changes did not return to normal even after clinical recovery.
Read 13 tweets
Oct 21
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.
The DNA carried blueprints for tixagevimab and cilgavimab - the antibodies used in Evusheld.
It was delivered intramuscularly, with short electric pulses (electroporation) that help DNA enter cells.
Read 11 tweets
Oct 20
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.
This is why COVID-19 can leave such a deep biological footprint. The virus doesn’t have to remain active to keep affecting you - it can alter the settings of your immune and metabolic genes in ways that persist long after recovery.
Read 22 tweets

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