This study suggests that in some patients, COVID-19 triggers a long-term process of vascular and cardiac injury that can gradually increase pulmonary pressure, strain the right ventricle, and raise the risk of death in the following years🧵
The study followed 480 hospitalized patients (240 moderate, 240 severe) for one year after discharge. It assessed heart function using echocardiography and measured biomarkers of vascular inflammation.
Feb 6 • 9 tweets • 2 min read
If normal population plasma truly carries more low-grade inflammation, this study hints at a fork in the road.
Either we lower the bar and call it a new normal,
or this is a hidden population burden that will surface later as comorbidities🧵
A new study on the cytokine IL-32 after COVID-19 points directly at this uncomfortable question.
Feb 6 • 10 tweets • 2 min read
Neurocognitive Long COVID doesn’t disappear.
Not with Omicron.
Not in a highly vaccinated population.
Even when most other organ-level signals fade🧵
A new population-level study from Singapore looked at 1.4 million COVID cases in a setting with >90% booster coverage.
Result - multi-organ Long COVID largely attenuates.
But the brain remains an exception.
Feb 5 • 17 tweets • 2 min read
This study does not tell us what exactly causes long COVID or ME/CFS, nor does it test clinical symptoms like PEM.
But it may tell us something just as important - what type of biological problem this likely is..🧵
The authors isolated immunoglobulins (IgG) from people with post-infectious ME/CFS, including post-COVID ME/CFS, and tested what these antibodies do to healthy cells.
Feb 2 • 15 tweets • 2 min read
This isn’t a new comparison.
For years, parallels between NeuroHIV and neuro-COVID/Long COVID have been discussed across fields.
What’s new is that they are now formally described as shared CNS mechanisms, not just analogy!🧵
Just a few years ago, parallels like
HIV - SARS-CoV-2
HAND - brain fog/neuro-LC
microglia - chronic inflammation
vasculature - cognition
were treated mainly as interesting analogies. With caution not to overstate them.
Feb 1 • 19 tweets • 3 min read
A new review links Alzheimer’s disease, Parkinson’s disease, and COVID-19 through a shared core - neuroinflammation + oxidative stress.
The same pathways, the same immune nodes, the same vulnerabilities of the brain🧵
Key players.
Microglia (the brain’s innate immune cells) and neutrophils (peripheral rapid responders).
When the blood–brain barrier (BBB) is disrupted, neutrophils enter the CNS and inflammation becomes self-amplifying.
Jan 31 • 18 tweets • 3 min read
Long COVID in children is often reduced to fatigue.
This study shows something far more concrete - measurable impairment in language skills - speaking, listening, and reading🧵
A new single-cell multiome study helps answer a key long-COVID question.
Where do the pathological monocyte programs seen later actually come from?
This paper maps how classical monocytes change already during the acute phase of COVID-19.
Jan 30 • 18 tweets • 3 min read
The choroid plexus (ChP) has become one of the most consistent findings in post-COVID and long COVID neuroimaging.
It is enlarged.
But larger alone doesn’t yet tell us what is actually happening🧵
A new paper in Alzheimer’s & Dementia moves the ChP story one step further.
It’s no longer just about volume - the authors also measure choroid plexus blood flow (CBF) and link it to cognition and biomarkers.
Jan 29 • 19 tweets • 3 min read
CD14 monocytes as the main pathological driver of long COVID?
A new Nature Immunology paper points to a clear biological signal in long COVID - CD14 monocytes - cells of the innate immune system🧵
The authors combined
single-cell RNA-seq
ATAC-seq (epigenetics)
plasma cytokines
functional stimulation assays
bronchoalveolar lavage (lung immune cells)
Crucially, they stratified patients by acute COVID severity - something many studies fail to do.
Jan 29 • 15 tweets • 2 min read
ME/CFS is sometimes framed as a body locked in stress mode.
The sympathetic nervous system permanently switched on.
Fight-or-flight with no way out.
It made sense.
Almost too much sense🧵
But the data have started telling a different story.
Not of a system that’s too strong -
but of one that’s exhausted.
Jan 28 • 20 tweets • 3 min read
Review paper.
At the center of Long COVID are three processes that reinforce each other -
persistent viral material, damage to the gut barrier, and chronic immune dysregulation. Together, they help explain why neurological and neuropsychiatric symptoms are so common and so persistent🧵
Viral persistence.
In a subset of people, fragments of SARS-CoV-2 - especially spike protein - persist for months or even years after the acute infection.
These viral remnants don’t need to actively replicate. Their continued presence is enough to keep the immune system switched on, similar to what we see in chronic viral infections like HIV.
Jan 27 • 18 tweets • 3 min read
An interesting metabolomic study suggests that one year after severe COVID-19, some people don’t just show altered metabolites in their blood -
they also carry chemically damaged proteins.
That’s not a sign of an ongoing reaction, but a trace of long-lasting biological stress🧵
Researchers followed patients who survived critical COVID-19 (ICU) and examined them 12M after discharge.
They compared those with Long COVID to those who fully recovered.
Using deep metabolomics and machine learning, they looked at cellular energy and molecular damage.
Jan 25 • 24 tweets • 4 min read
1. COVID-19 infection during pregnancy is not a neutral event.
Inflammation, viral proteins, and especially COVID-specific impairment of placental blood flow can affect fetal development - and abnormalities in exposed newborns are being reported with increasing consistency across studies.
That infection during pregnancy increases the risk of neurodevelopmental difficulties - in speech, motor skills, attention, and learning - has been known in public-health and medical circles for years.
Mothers were simply not told.
This wasn’t ignorance.
It was a decision to downplay the risk.
Jan 25 • 23 tweets • 3 min read
Long COVID is often described as fatigue, sleep disruption, and brain fog.
This preprint study asks a concrete question - does SARS-CoV-2 disrupt specific brain control systems that could explain these symptoms?🧵
They used two mouse models of SARS2
K18-hACE2 mice (low dose - survival - follow-up up to 90 days)
Wild-type BALB/c mice infected with mouse-adapted SARS2 (MA10), also followed long-term.
Jan 24 • 16 tweets • 2 min read
The outcome of SARS-CoV-2 infection seems to depend more on the quality of early innate immunity (pDC + NK cells) than on the strength of the antibody response.
A 2026 immunology study helps explain why.🧵
The authors compared two immune profiles:
Hospitalized COVID-19 patients
PCR-confirmed infection, mild to severe disease
Healthcare workers without proof of infection
PCR-negative and seronegative (IgM/IgG), unvaccinated (2020)
Jan 22 • 20 tweets • 3 min read
Over the past few years, many MRI studies after COVID have reported structural brain changes -
thicker cortex here, altered volumes there, sometimes even a larger hippocampus.
The problem wasn’t whether changes exist.
It was why the findings rarely line up🧵
A new study suggests a reason.
We’ve been looking for the same region to be abnormal in everyone.
But post-COVID brain changes don’t work like that.
They seem to be network-based, subtle, and individually distributed -
which means you’re more likely to see the signal once you stop thinking in isolated brain regions.
Jan 21 • 12 tweets • 3 min read
Infection of the adaptive immune system as a hidden disease mechanism?
We often explain severe or chronic viral illness as excessive inflammation.
But a new FIP (feline infectious peritonitis) study suggests something deeper -
Coronaviruses may directly disrupt T and B cells - the core of adaptive immunity.🧵
What we thought for years?
FIPV = a macrophage-restricted virus.
What this study shows?
Viral RNA and protein in T and B lymphocytes
subgenomic RNA (sgRNA) inside T cells - a marker of active replication
That’s not just background inflammation.
Jan 20 • 18 tweets • 3 min read
Four years after infection, most people treated for long COVID in a specialist clinic still hadn’t returned to their previous level of health🧵
This prospective cohort study followed 3,590 people with long COVID for up to four years in a specialist post-COVID clinic in London.
Most patients were not hospitalised during their acute infection, the majority were working-age adults, and nearly two-thirds were women.
Jan 19 • 21 tweets • 3 min read
Severe COVID doesn’t end with a negative test.
In the worst cases, we see epigenetic rewiring of genes that control mitochondria - the cell’s energy system. And once that switch flips, it doesn’t always flip back🧵
This isn’t a random epigenetic signal.
The changes concentrate in promoters of genes controlling respiratory chain complexes I and IV - the core machinery that turns oxygen and nutrients into usable energy (ATP).
Jan 18 • 15 tweets • 2 min read
A new study in Journal of Clinical Medicine shows that after COVID-19, many patients have persistent impairment of oxygen transfer in the lungs (DLCO/KCO) - lasting 12 to 22 months, even when basic spirometry looks almost normal🧵
Key point?
FEV1 remains largely stable, while FVC improves only slowly over time.
This doesn’t look like classic airway obstruction. It points instead to restrictive and diffusion-level damage.
