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Zdenek Vrozina Profile picture
Zdenek Vrozina
@ZdenekVrozina
Health Care Consulting
Jul 10 • 16 tweets • 3 min read
An Italian group took stomach lining biopsies from people with Long COVID and counted the nerve fibers in them. Under endoscopy the mucosa looked normal. Under a fluorescence microscope, roughly half the fibers were gone.🧵 12 patients with symptoms lasting more than 12 weeks, 8 controls no prior infection who were having a gastroscopy anyway. Biopsies from the fundus and antrum, taken 21 weeks after a negative swab. A blinded operator.
Jul 8 • 20 tweets • 3 min read
The study in Clinical Ophthalmology - LISTEN, 595 people with long COVID.
57% report new ocular symptoms - blurred vision, dry eyes, floaters or flashes. The headline isn’t really about the eyes🧵 The eyes here work more like a warning light than a site of primary damage. People who report ocular symptoms carry a heavier overall illness picture across the board.
Jul 7 • 16 tweets • 3 min read
A German study followed 74 children and teens with severe long COVID for up to 3 years after infection, measuring their immune systems repeatedly. The finding worth unpacking - that immune picture kept shifting over time. It wasn't frozen in place.🧵 In the first year an antiviral signature dominated - signalling IFNα, IL-13, IL-33.
By years 1-3 that signature had dropped back to the levels seen in healthy kids. At first glance, that looks like recovery.
Jul 1 • 15 tweets • 3 min read
New study out of Amsterdam UMC asks a question most Long COVID imaging papers don’t tackle at once - does inflammation in the brain actually track with how well different brain regions talk to each other? 45 people, roughly 27 months post-infection!🧵 TSPO PET is a scan that lights up wherever immune cells in the brain (microglia) are activated - basically a map of where inflammation is happening. This version is fully quantitative, with blood sampling during the scan, not a shortcut estimate.
Jun 30 • 17 tweets • 3 min read
Severe COVID at least temporarily (years) weakens the part of the immune system that keeps dormant and opportunistic pathogens in check.
3.6 mio dataset from Chile shows this on a textbook example - tuberculosis🧵 People hospitalized with COVID had more than an eightfold higher risk of TB flaring up over the following year.
Jun 28 • 19 tweets • 3 min read
COVID ages the brain. But we keep hitting the same wall - how do you prove it when the brain changes over years and we only have data spanning months?
A new study tried to get around that wall through a completely different door. Genetics.🧵 The logic is clever. Everyone gets their genes shuffled at random at conception - and some of that shuffle makes people more prone to severe COVID.
Jun 27 • 13 tweets • 3 min read
If you wear a Fitbit or a smartwatch, you may have noticed your HRV drop and your resting heart rate climb after COVID. Data from 1,475 people in the RECOVER cohort now confirm that pattern objectively - from passively collected sensor data🧵 The study took passive wearable data from 1,475 people a median of ~21 months (!) after infection and matched it against a symptom questionnaire. The differences between groups are small but statistically solid.
Jun 25 • 15 tweets • 3 min read
Researchers built a mouse with a human immune system to finally watch how human defenses fight COVID. They expected the virus to get wiped out. Instead, the human immune cells helped it spread from the lungs into other organs and muffled the body's own early alarm system🧵 Older COVID mouse models had two problems. The virus's entry lock - the ACE2 - was cranked up to artificial levels, so the mice died of things we don't see in people. And their human T cells developed badly and attacked the mouse's own body.
Jun 23 • 21 tweets • 4 min read
New study in Journal of Sleep Research links long COVID to a higher burden of prodromal Parkinson's like features. 11,261 people, 16 countries.
The headline is weaker than it looks - but there is the one finding in this paper that should genuinely scare you, and almost nobody is quoting it 🧵 The main finding is mostly circular. The prodromal PD score is built from cognitive impairment, fatigue, depression, dysautonomia, anosmia, constipation. Those are long COVID. They renamed the long COVID symptom cluster prodromal PD and found long COVID predicts it.
Jun 22 • 13 tweets • 2 min read
In people with long COVID, arterial stiffness in the large vessels looked no different from people who’d recovered cleanly.
The deficit sits one level down - in the smallest vessels, and specifically in how fast they can react.🧵 A new paper from Tübingen measured microvascular reactivity - how quickly a muscle re-oxygenates after its blood supply is cut off for a few minutes and then released. That re-flooding step is called reperfusion. A near-infrared sensor on a forearm muscle tracks how oxygenated the tissue is throughout.
Jun 19 • 13 tweets • 2 min read
139 kids who'd had COVID. Half of them turned up with autoantibodies - antibodies that attack the body's own tissues. In uninfected kids, only 14%. And it barely mattered whether the child had been hospitalized with pneumonia or had next to no symptoms. 🧵 The study sorted the kids by how their infection went - mild/asymptomatic, severe COVID needing hospitalization, and MIS-C hyperinflammatory syndrome that shows up weeks after infection and hits several organs at once. Plus a group of healthy controls.
Jun 18 • 11 tweets • 2 min read
New study. In some people, a mild case of COVID seems to leave a hidden edit in how their cells manage their own RNA - and it doesn't fully reset once the virus is gone. Another possible clue to why some bodies don't bounce back the same. 🧵 Your DNA is the master copy. RNA is the working copy your cells actually read to build proteins. A family of enzymes called ADAR can edit letters in that working copy - swapping an A so it now reads as a G - without ever touching the DNA.
Jun 14 • 16 tweets • 3 min read
Could the real trigger for Long COVID POTS be the immune system mistaking your own cells for the enemy? A new preprint makes the case that monocyte oxidative stress - not lingering virus - keeps the immune system switched on. Vanderbilt, 25 patients vs 15 recovered. 🧵 The headline finding.
Patients carry about 3× more doublets in their blood - T cells and monocytes stuck together. These used to get written off as a lab artifact. Turns out they're real, functional contacts where the cells are actively talking to each other. The body is working on something.
Jun 13 • 17 tweets • 3 min read
Independent virus families - different genomes, life cycles, target tissues - keep ending up at the same two points in the brain. They switch on the same inflammation machinery, and they jam the cell's protein clean up system. If so, the damage is mostly the body's reaction, not the virus itself. 🧵 This is the core argument of a new review - one of the few that looks at post-viral brain symptoms through mechanisms shared across many viruses, instead of one virus at a time.
Jun 11 • 17 tweets • 3 min read
A multi-omics paper on long COVID in Frontiers in Immunology deserves more attention than it got. The through-line is uncomfortable - the cellular power supply stays switched off long after the acute phase is over.🧵 It's an integration of existing public datasets under one roof. Syrian hamsters (muscle, heart, kidney, lung, 8 brain regions, out to 61 days post-infection) + human cohorts - immune cells, muscle biopsies, autopsy brain, and longitudinal serum stretching to 24 months. Different tissues, different species.
Jun 11 • 12 tweets • 2 min read
How many Americans died who wouldn't have - if America were France or Japan?
The answer - 14.7 million over the past four decades.
And that number is still climbing🧵 This comes from a study published in 2025 in JAMA Health Forum (Bor et al.). The researchers compared US death rates to 21 other wealthy countries - Canada, Japan, Germany, France, the UK and more - from 1980 through 2023.
Jun 10 • 17 tweets • 3 min read
New Mayo Clinic study.
Brain hypometabolism in long COVID still showing up 2 years post-infection. This finding keeps replicating. It matters clinically. But there’s a lot worth unpacking. 🧵 Reduced brain metabolic activity in LC isn’t a one-lab quirk. Guedj 2021, a French multicenter study across three centers (n=143), pediatric case series - it keeps showing up across countries and cohorts.
Jun 9 • 25 tweets • 4 min read
A new review pulls the neurobiology of Long COVID into a pretty strong map.
Neuroinflammation here is not treated as one isolated process. It’s the place where viral persistence, glia, BBB, blood vessels, mast cells, vagus nerve, metabolism, and unstable brain networks all meet🧵 It’s an expert review - a synthesis of mechanisms, biomarkers, and possible therapeutic directions.
Jun 8 • 25 tweets • 5 min read
A genuinely interesting study.
Researchers from Johns Hopkins looked at how SARS2 infection changes the cardiac autonomic nervous system - how the heart is regulated through the sympathetic and parasympathetic branches.
It’s not one fixed state.
It’s a process.
In three phases🧵 Why does this matter?
Because dysautonomia is one of the common features of Long COVID -
palpitations, dizziness, fatigue, orthostatic intolerance, POTS etc
The autonomic nervous system helps regulate heart rate, blood pressure, breathing, digestion, the body’s ability to adapt to stress.
Jun 6 • 22 tweets • 3 min read
Viral proteins can activate the same pathways after infection that connect neuroinflammation, synapse loss, tau, alpha-synuclein, and broken cellular cleanup.
That’s why parallels with other viruses, including HIV, matter.
A new review tries to put this whole story together. 🧵 The main point is not that SARS2 has to keep massively replicating in the brain.
The authors suggest a protein-as-pathogen model.
Viral proteins themselves may act as long-term triggers, keeping nervous tissue stuck in innate immune activation, stress, and poor cellular cleanup.
Jun 5 • 20 tweets • 3 min read
Does the brain always return to baseline after COVID?
A new multimodal MRI study suggests the answer may be - not always.
After infection, some brains may remain in a different network state - and we still do not know if that state is temporary, compensatory, or maladaptive🧵 The important part is not one single MRI finding.
The strength of this study is that it combines three MRI layers
structural MRI - grey matter volume,
diffusion MRI - white-matter microstructure,
resting-state fMRI - functional connectivity.