Zdenek Vrozina Profile picture
Health Care Consulting
Jul 31 17 tweets 3 min read
A new persistence study tracks SARS2 in Syrian hamsters for the longest span published so far. A full year after infection. The question is simple - does the virus persist in the body after the acute phase? The answer is more precise than yes/no.🧵 A year is roughly half a hamsters typical lifespan - the animals were also infected as young adults (8-10 weeks), so persistence was tracked across essentially their whole adulthood.
Jul 28 14 tweets 3 min read
A new mouse study gives us a hard close-up of something long COVID data keeps hinting at.
SARS2 gets into the brain, clears out within a month - and the damage it leaves behind doesn’t just persist, it keeps growing. The virus clears out and leaves scorched earth behind it🧵 K18-hACE2 mice, Delta, tracked at 6/14/30 days post infection.
Day 6 - virus peaks in the brain (both N-protein and infectious particles).
Day 14 - only half the animals still have it.
Day 30 - undetectable.
The classic pattern - acute neuroinvasion, then cleanup.
Jul 28 17 tweets 3 min read
Two variants that went on to dominate the world - BA.2.86 and its descendant JN.1 - replicate worse in the airways than the variant they displaced.
But better in the small intestine.
New work from HKU shows viral fitness isn’t a single number - it’s a trade off between tissues.🧵 We each carry a different mix of past infections and vacc. That immune background masks what a variant can intrinsically do. The authors got around it by testing replication in tissue models with no immune system - where only the virus’s own biology shows through.
Jul 26 23 tweets 5 min read
COVID & amyloid.
Since 2022, a growing body of research has taken one possibility seriously - that amyloid - proteins refolded into clumped, degradation resistant aggregates plays a role in the pathology of COVID/long COVID. This isn't a fringe idea. At least five independent labs stand behind it, plus a review in Lancet Neurology.🧵 Two 2022 papers laid the groundwork. Nyström & Hammarström found seven amyloidogenic segments within the spike protein. Charnley identified peptides from SARS2 that self-assemble into structures toxic to neurons. Both cleared the formal bar - the dye ThT, Congo red with birefringence, and fibrils under the microscope. That's the threshold the field sets for calling something amyloid.
Jul 22 18 tweets 3 min read
Interferon works against SARS2. In these experiments it knocks infection down by 80 to 96%.
But it doesn’t cut evenly. What it leaves standing is the spread that runs by a route it can’t reach.
A new NIAID paper shows what that did to spike evolution🧵 The virus has two options for getting into the neighbouring cell.
Package itself into a virion, swim out, enter again. Out there it’s exposed to everything waiting for it.
Or fuse the infected cell with its neighbours into one multinucleated cell - a syncytium - and never go outside at all.
Jul 13 16 tweets 3 min read
SARS2 doesn’t have to infect the brain to damage it. A new review in Frontiers Neurol. lays out how - and builds the whole thing on a cell long COVID coverage almost never mentions.
The mast cells in your meninges.🧵 Most post-mortem brains don’t show the virus productively infecting neurons or microglia. So where’s the damage coming from? The answer the review builds toward - it isn’t replicating virus driving this. It’s spike protein that stays behind.
Jul 13 17 tweets 3 min read
New interesting mouse study out of Barcelona follows K18-hACE2 mice for 60 days after SARS2 infection. The trick - a deliberately low dose, so most animals survive the acute phase and can actually be followed this long. The goal - catch what’s left once acute COVID clears🧵 They recovered from mild COVID. Two (mouse) months later - nothing in the blood, but persistent immune dysregulation in tissue and a shrunken vagus nerve. A standard blood draw would’ve sent them home healthy.
Jul 11 16 tweets 3 min read
A Toronto group took the same brain scan used to track Parkinsons - and pointed it at people with long COVID.
Dopamine nerve terminals in the striatum - reduced. Down in the range you’d see in mild-to-moderate Parkinson’s. Lancet family.🧵 The scan is DTBZ PET. It measures VMAT2 - the density of dopamine neuron terminals across three parts of the striatum. One for motivation, one for movement, one for memory.
This is an established Parkinson’s tool. Not something rigged up for COVID.
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.