Zdenek Vrozina Profile picture
Mar 31 13 tweets 2 min read Read on X
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.
The most striking part is how much was missed before death. Among people with influenza detected post mortem, only 17% had been diagnosed with influenza while alive.
That matters because what gets recorded as cardiac death, respiratory failure, or general decline may, in many cases, have had a hidden viral trigger helping push a frail patient over the edge.
The study does not claim every virus detected was the direct cause of death - but it strongly suggests we are overlooking a major part of the story.
These viruses are not harmless background noise. They can worsen an already fragile situation, destabilize chronic illness, and become part of fatal outcomes even when they never make it into the headline diagnosis.
The signal was especially strong in long-term care facilities, where any respiratory virus was found in 52.3% of deceased residents!
That is exactly where transmission is easier, patients are more vulnerable, and missed infections can carry the heaviest consequences.
So ignoring such a high prevalence would be a mistake. These infections are being underdiagnosed in life and undercounted in death.
The practical takeaway is simple.
Test more, think of viral etiologies more often, and stop assuming that if a patient looks cardiac, pulmonary, or just frail, infection is no longer central to what is happening.
And this study comes from the pre-COVID era. Since then, SARS-CoV-2 arrived. More severe, poorly tested, devastating in care homes, and far too often met with delayed, limited, or badly implemented antiviral access.
If we were already underestimating how flu and other respiratory viruses contribute to fatal decline, COVID only made that blind spot bigger. We need better testing, earlier recognition, and much better treatment access for the people at highest risk.
Trobajo-Sanmartín at al., Prevalence of influenza and other respiratory viral infections in deceased persons: a population-based observational study over four influenza seasons. clinicalmicrobiologyandinfection.org/article/S1198-…

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More from @ZdenekVrozina

Jul 26
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.
Since then, follow ups have accumulated across groups. Larsson 2023, cross-seeding with prion and Aβ, Sanislav 2024, polymorphs and neurotoxicity, the Hansmann branch α-synuclein, Aβ, and Follmer/Gemignani, α-synuclein and Parkinson's. The signal converges from several independent directions.
Read 23 tweets
Jul 22
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.
Interferon induced defence proteins mostly target the first route. Entry of an incoming virion.
A membrane fusing between two cells isn’t an incoming virion.
One route gets choked hard, the other much less.
Read 18 tweets
Jul 13
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.
The most solid, independent part of the review story? Swank 2023. Full-length spike in the plasma of 60% of people with PASC, up to 17 months out - nothing in acute patients in week one. Peluso 2024. Persistence past 14 months, with levels tracking markers of immune activation.
Read 16 tweets
Jul 13
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.
At the group level, infected and control animals didn’t differ on behavior. At all. The signal only shows up in individual z-scores - a subset of animals carries the damage while the rest look normal. It’s not all the mice got worse, it’s some got notably worse.
Read 17 tweets
Jul 11
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.
24 people with long COVID, 24 age matched healthy controls. Lower signal in all three regions. Magnitude comparable to mild-to-moderate PD - and the putamen sits at the level you see in RBD (REM sleep behaviour disorder, most specific early precursor to synucleinopathy). @DavidJoffe64_2
Read 16 tweets
Jul 10
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.
Two stains. PGP 9.5 marks all nerve fibers. VIP marks a subset of autonomic fibers that the authors treat as cholinergic. Software then reconstructs the nerves in 3D and computes fiber length per volume of tissue.
Read 16 tweets

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