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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A heart attack after COVID may not look like the classic heart attack we usually imagine.
A new core-lab study of patients with NSTEMI + COVID-19 suggests something more diffuse. Not just one blocked artery, but a blood-clotting and vessel inflammation problem🧵
First, two key terms.
STEMI is the type of heart attack where the ECG shows ST-segment elevation. It often means a major coronary artery is suddenly blocked.
NSTEMI is a heart attack without that classic ST elevation. It can be less obvious on ECG, but it is not minor.
So STEMI is often like a main pipe suddenly being blocked.
NSTEMI can be more complex. Partial blockage, smaller clots, multiple narrowed vessels, poor microvascular flow, or the heart being stressed by illness.
But COVID can add another layer.
For 2025, the societal cost of Long COVID and ME/CFS in Germany is estimated at €64.4 billion - about 1.44% of GDP.
For Czechia, this would roughly translate to around CZK 120 billion per year if we apply the same share of GDP - 1.44% of the Czech economy.
A simple population-based conversion would produce a higher number (200 billion), but that is an overestimate.
This should matter to you, @strakovka.
Because this is what poor public health policy costs. Ignoring prevention, ventilation, surveillance, post-COVID care, and the long-term damage caused by repeated infections.
A new systematic review looked at what happens to the heart after COVID - not during the acute infection, but months later.
The key point:
A normal ejection fraction does not always mean the heart is completely unaffected.🧵
In people assessed more than 12 weeks after PCR confirmed COVID - especially those with persistent cardiopulmonary symptoms - there is evidence of subtle, and sometimes persistent, cardiac involvement.
This may show up as
higher BNP/NT-proBNP
reduced LV-GLS
abnormalities on cardiac MRI
while LVEF often remains normal
Exertion and PEM.
A new paper studied people with long COVID using a 2-day (!) submaximal CPET protocol, combined with NIRS measurement on the calf muscle.
The authors looked at what happens to breathing, performance, and muscle oxygenation during repeated exertion🧵
The key finding.
In the long COVID group, muscle tissue oxygen saturation (TSI%) initially increased during exercise, but it did not stay elevated for as long as it did in controls. (Thomas 2026)
On day 2, this pattern was even worse. In long COVID, TSI% stayed above resting levels for a shorter period, while controls maintained elevated muscle oxygenation more effectively during exercise.
COVID-19 creates a state of immune dysregulation where the body may lose control over things it normally keeps suppressed - latent viruses, especially herpesviruses, and possibly even dormant cancer cells.
A new study on EBV and CD8 T cells fits into this bigger picture.🧵
The point is not simply that EBV can reactivate during COVID. We already have quite a lot of evidence for that.
In hospitalized patients with acute COVID, EBV reactivation was very common - around 68-73% - and it was seen not only in critical cases, but also in moderate disease.
The authors looked at EBV, CMV, HHV-6A and HHV-6B.
EBV dominated.
CMV and HHV-6B were detected only at low frequencies.
HHV-6A was not detected at all.
So this does not look like just random viral noise. EBV stands out.
In this cohort, children exposed to SARS-CoV-2 in utero showed higher rates of developmental delay and were also more likely to screen positive on an autism screening tool than pre pandemic controls🧵
The developmental delay signal comes from the group’s earlier work in the same cohort. In the abstract, the authors cite a rate of 11.6% in 172 exposed children versus 1.6% in 128 pre pandemic controls.
The newer clinical piece in this paper is the autism screening result. Among 218 SARS2 exposed children, 22 screened positive on M-CHAT-R/F (10.1%). In the control group, 30 of 527 screened positive (5.7%).