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Zdenek Vrozina Profile picture
Zdenek Vrozina
@ZdenekVrozina
Health Care Consulting
Apr 18 • 16 tweets • 3 min read
We now have a complementary study that helps extend the picture. If the first paper suggests post-COVID biology may exist on a spectrum, this second one suggests recovery itself may also be real, prolonged, and only partial.🧵 This was a 2 year longitudinal proteomics study of hospitalized COVID survivors. The researchers profiled plasma at 6 months, 1 year, and 2 years after symptom onset and compared it with matched healthy controls.
Apr 17 • 17 tweets • 3 min read
A new Scientific Reports study adds an important nuance to the long COVID conversation. The biggest difference was not between people with PCC and without PCC, but between uninfected people and everyone who had recovered from SARS2🧵 Long COVID may be part of a broader post-infectious biological spectrum, where symptomatic PCC represents the more clinically visible end of a continuous dysregulation rather than a completely separate category.
Apr 16 • 22 tweets • 4 min read
A new study asks a deceptively simple question - is Long COVID just a slower recovery, or is it a persistent immune disorder? Their data point toward the latter !🧵 For this single-cell analysis, the authors selected 9 women from a prospective cohort of patients hospitalized with COVID-19. Blood was collected during acute infection, at 3 months, and again 18-24 months later. Some recovered without long-term complications. Others developed pulmonary or cardiovascular Long COVID.
Apr 15 • 15 tweets • 3 min read
A new first trimester study makes an important point. Even when direct detection of SARS-CoV-2 in placental tissue is minimal, the early maternal-fetal environment can still be meaningfully disrupted - immunologically and developmentally🧵 Biological harm does not have to depend on heavy, obvious viral presence inside the tissue itself.
Apr 14 • 24 tweets • 4 min read
Very small study, but a genuinely interesting one on long COVID.
After reinfection, the biology did not simply replay the first infection - and in this cohort, the booster did not worsen the measured inflammatory/neurology protein profile🧵 The authors measured 182 inflammatory and neurology related proteins in plasma -
6-9 months after primary infection
after a booster
after breakthrough infection.
In a subset, they had longitudinal samples at 3 timepoints, which makes the paper much more interesting than a simple one time comparison.
Apr 12 • 23 tweets • 4 min read
COVID-19 is not just a story of inflammation. This review argues that it is also a story about what SARS2 does to mitochondria - and how that can turn infection into energy failure, cell injury, and worse oxygenation. This is an important mechanistic review🧵 Mitochondria are not framed here as passive bystanders damaged late in severe illness. In this model, they are active participants in disease - they shape ATP production, ROS, apoptosis, and oxygen sensing.
Apr 11 • 18 tweets • 3 min read
This interesting paper lays out a very specific idea for how severe COVID-19 may be driven not only by the virus itself, but by the way the immune system handles what the virus leaves behind🧵 The starting point is simple.
SARS2 can leave behind viral RNA and nucleocapsid protein (N). N naturally binds viral RNA, and during infection people also make antibodies against N.
Apr 10 • 7 tweets • 2 min read
Can Long COVID show up in a blood sample?
A new preprint @resiapretorius suggests it might. Researchers found much higher platelet-monocyte aggregates in people with Long COVID than in healthy controls - about 29% vs 4.6%🧵 That is a striking signal, and it hints that Long COVID may leave a measurable trace in blood.
In healthy controls, a monocyte was more likely to have just one platelet attached. In Long COVID, researchers more often saw multiple platelets attached to a single monocyte.
Apr 9 • 16 tweets • 3 min read
Long COVID research badly needs studies that move beyond description and toward intervention. This is why this preprint is worth attention. It starts to sketch a possible treatment path.🧵 A new preprint is interesting because it points to something important
a potentially treatable biological mechanism.
Not a clinical breakthrough. More like a promising preclinical proof of concept.
Apr 9 • 12 tweets • 2 min read
Do you have hypertension?
This study in Nature suggests that for people who already had hypertension before getting COVID, the infection was linked to a higher long-term risk of serious cardiovascular events.🧵 In people with hypertension, an infection can leave behind - or speed up - processes that raise the risk of cardiovascular disease over the months and years that follow.
Apr 7 • 12 tweets • 2 min read
Another piece of the puzzle. Post-COVID changes are not just an isolated problem affecting a few unlucky individuals. They appear to have consequences at the population level🧵 A striking headline from Austria - 4 in 10 people report smell or taste problems.
That figure comes from a new cross-sectional survey of 2340 adults in Austria, Germany, and Switzerland looking at self-reported smell and taste disorders after the COVID era.
Apr 7 • 13 tweets • 2 min read
The Karaviti study is finally in print, which makes this a good time to revisit it. It shows that subclinical myocardial injury in children after COVID-19 may not be something exceptional🧵 The key point is often missed. This was not mainly a comparison of children with Long Covid versus children without Long Covid. It compared
children after COVID-19
healthy controls without prior SARS-CoV-2 exposure
Apr 6 • 9 tweets • 2 min read
This study suggests a possible mechanism for how SARS-CoV-2 could harm neurons in the inner ear.
Not mainly through inflammation, but potentially through a more direct effect on spiral ganglion neurons, involving disrupted mTOR signaling, abnormal stress granules, and eventually - apoptosis🧵 That matters because spiral ganglion neurons are not some minor supporting cells. They are the neurons - that carry sound information from the cochlea into the auditory pathway.
If they are damaged, the problem is not just in the ear. It affects the neural transmission of sound itself.
Apr 4 • 13 tweets • 2 min read
A new paper looks at shared molecular mechanisms between COVID-19 and Parkinson’s disease. It does not show that COVID causes Parkinson’s.
What it does ask is whether the two conditions share biologically meaningful pathways🧵 The authors identified 77 overlapping differentially expressed genes across COVID-19 and Parkinson’s datasets. The main signal points to inflammation-related pathways plus signs of dopaminergic neuron dysfunction!
Apr 3 • 14 tweets • 2 min read
A new population based study from Stockholm sends a pretty troubling signal.
During follow-up, a cardiovascular event occurred in 20.6% of men and 18.2% of women with diagnosed long COVID.🧵 In the control group without long COVID, the numbers were much lower. 11.1% for men and 8.4% for women.
Apr 2 • 25 tweets • 4 min read
A new 2026 paper looks at a possible mechanism behind rare myocarditis after COVID-19 mRNA vaccination.
Not vaccines broadly damage the heart.
More like
some people may be biologically more vulnerable than others🧵 The paper’s central idea is mitochondrial vulnerability.
In simple English
your mitochondria can seem mostly fine under normal conditions, but still handle stress badly when the system gets pushed.
Apr 2 • 13 tweets • 2 min read
This new important preprint study makes a strong mechanistic case that the SARS-CoV-2 E protein localizes to mitochondria and is linked to concrete mitochondrial dysfunction🧵 It pushes E beyond the idea of being just a structural protein involved in viral assembly. The paper suggests it may also directly disrupt host-cell function at the mitochondrial level.
Mar 31 • 13 tweets • 2 min read
Hidden driver of mortality. A new study makes an uncomfortable point very clear. Respiratory viruses are probably involved in far more deaths than we usually recognize in day-to-day clinical practice or in official cause-of-death statistics🧵 Across 4 influenza seasons, a respiratory virus was found post mortem in 36.4% of deceased people. Influenza alone was present in 11.0%. It was not just flu either - rhinoviruses, common human coronaviruses, and RSV were also frequent.
Mar 30 • 17 tweets • 2 min read
A bystander apoptosis. The study in Nature argues that Omicron can drive the death of nearby, uninfected T cells. This paper shows an HIV-like pattern of immunopathology.🧵 A new paper suggests something important about severe Omicron cases.
The damage may not come only from the cells the virus infects directly.
It may also come from the immune cells caught in the crossfire.
Mar 28 • 21 tweets • 4 min read
Why might insulin resistance go up after COVID? Probably not because of one single cause, but because of a whole network of inflammatory and metabolic changes. A new narrative review.🧵 Some people seem to have worse blood sugar control and higher insulin resistance after COVID. What this paper argues is interesting - it’s probably not one clean, simple mechanism. It’s more like a web of biological processes that can keep reinforcing each other.
Mar 25 • 12 tweets • 2 min read
Patient-derived IgG in Long COVID appears functionally pathogenic - and in some cases, this autoreactivity persists for years🧵 At the heart of the paper is a pretty important question. We already know that Long COVID has often been linked to autoimmunity, but that alone does not tell us whether these antibodies are actually doing harm or whether they are simply a byproduct of the illness.