COVID didn’t end - it changed the baseline of how often people fall ill, miss work, and drop out of the labor force. A new JAMA study shows the US now lives in a permanent flu-season mode, all year round🧵
COVID-19 has created a new year-round baseline of illness - its effects persist even without major waves or restrictions, pointing to chronic impacts from ongoing infection or post-infectious conditions, including long COVID.
This new health environment means lower productivity and a greater need for worker protections such as paid sick leave, improved ventilation, and infection prevention at workplaces.
Sick leave remains 12.9% higher than before the pandemic - about 1.29 million absences per month vs 1.15 million prepandemic (+140,000 monthly).
These absences closely track SARS-CoV-2 levels in wastewater, not influenza or RSV - showing that illness now stays high throughout the year, similar to pre-pandemic flu season levels!
Occupational disparities persist.
Jobs with low remote-work potential +8.1% absences
Jobs with high physical proximity (eg healthcare, service work) +12.5%
Lasting exits from the labor force - workers are 13.1% more likely to leave the workforce after a health-related absence than before the pandemic.
Sum:
Even after the pandemic officially ended, health-related absences and labor force exits in the US remain significantly elevated and closely tied to ongoing SARS-CoV-2 circulation. COVID-19 has effectively reset the baseline of population health, leaving enduring economic and workforce consequences.
It’s almost absurd how public health keeps juggling flu statistics while ignoring the far more profound social impacts of SARS-CoV-2 - which has, in the meantime, fundamentally reshaped how often people get sick and how societies function. @JakubHlavka
The next crisis won’t come from a new variant only, but from healthcare systems strained by the long tail of post-COVID illness - full hospitals, overrun clinics, and an exhausted workforce. @szupraha @ZdravkoOnline
Rarely have so few people caused such enormous economic damage as those who have been steering the public health response to COVID-19.
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New preprint from Harvard & Massachusetts General Hospital -children with Long COVID show markedly increased levels of fibrinaloid microclots in their blood!
The highest levels appear in those with persistent SARS-CoV-2 spike protein in circulation🧵
Long COVID affects roughly 1 in 5 children after SARS-CoV-2 infection.
Common symptoms include fatigue, brain fog, pain, and shortness of breath.
Diagnosis remains largely clinical - we still lack objective lab biomarkers for pediatric LC.
To address this, the team led by Daniel Irimia and David Walt developed a microfluidic device that can quantifyfibrinaloid microclots - tiny, fibrin-like clots resistant to normal breakdown (fibrinolysis).
These structures can obstruct microcirculation and reduce tissue oxygen delivery.
The study, conducted in a mouse model, shows that SARS-CoV-2 infection can alter epigenetic information in sperm - specifically the profile of small noncoding RNAs passed on at fertilization - and that these changes can be transmitted to the offspring🧵
These changes may influence the development of the nervous system and the stress response of the offspring, independently of the DNA sequence itself.
Male mice infected with SARS-CoV-2 were mated with uninfected females four weeks after recovery.
Their offspring showed no signs of infection, but exhibited changes in behavior and gene expression.
Post-COVID depression isn’t weakness.
It’s biology.
A landmark, important study shows how the virus leaves a measurable molecular trace - in the very proteins that protect your brain from degeneration🧵
A new study in Translational Psychiatry shows that psychiatric symptoms after COVID-19 aren’t just psychological.
They have a biological signature - measurable changes in blood proteins linked to the brain, metabolism, and immunity.
People who developed new depression, anxiety, PTSD, or insomnia after COVID showed distinct biochemical profiles compared to those who recovered fully or had other long COVID symptoms.
It’s not psychology.
It’s neurobiology.
7-12% of patients recovering from moderate to severe COVID-19 show persistently low counts of B cells, CD4 T cells, and Tregs, even after clinical recovery.🧵
This sustained adaptive immune deficit may represent a important mechanism underlying Long COVID, resembling immunological patterns seen in chronic infections such as HIV and EBV.
The authors highlight a possible link with low serotonin levels, which support B and T cell proliferation - a hypothesis drawn from the work of Wong et al., 2023.
Yes, we wrote about this study. It is important.
A study from Cambridge in Brain shows that even months after COVID-19, survivors still carry measurable inflammation-related changes in the brainstem - the part of the brain that keeps you breathing, awake, and alive🧵
Using ultra–high-field 7 Tesla MRI, researchers found abnormal magnetic signals (quantitative susceptibility mapping, QSM) in key brainstem areas.
medulla oblongata
pons
especially in the raphe nuclei and reticular formation - core hubs for breathing and autonomic control.
What does that mean?
Higher magnetic susceptibility usually reflects iron accumulation, microglial activation, or loss of myelin - all signs of neuroinflammation.
These changes weren’t random - they tracked with how severe the original infection was.
SARS-CoV-2 can create an oncogenic-like cellular environment - switching off tumor suppressors, activating growth pathways, reshaping epigenetic control, and fueling inflammatory metabolism.
If these effects persist, the virus could act as a cofactor in carcinogenesis🧵
The authors don’t claim SARS-CoV-2 causes cancer like HPV or EBV.
They show that the virus interferes with the same cellular checkpoints and signaling pathways commonly disrupted in tumors.
It’s about strong oncogenic potential, not direct oncogenicity.
In normal cells infected with SARS-CoV-2, scientists observed changes resembling those seen in cancer cells.
Loss of tumor suppressors (p53, pRB), activation of growth and survival cascades (PI3K/AKT, MAPK), and disruption of epigenetic balance.