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.
Jan 16 • 7 tweets • 2 min read
One of the strongest - and most concerning - studies so far. A true before/after design, a clear tau signal in persistent neurological symptoms, and nearly half exceeding Alzheimer’s research pTau-181 thresholds🧵
Related evidence. A large UK Biobank longitudinal analysis in Nature Medicine - Duff et al., 2025 -compared plasma Alzheimer’s-related biomarkers before vs after SARS-CoV-2 infection (with matched controls).
Jan 14 • 15 tweets • 3 min read
In people with neurological long COVID, infection is followed by a significant increase in pTau-181, and in a subset this is accompanied by changes in amyloid markers!
This biomarker pattern is compatible with tau-related pathology and may point to a worse long-term prognosis🧵
A new prospective study in eBioMedicine followed 227 individuals with blood samples collected before and after COVID-19.
That matters - this isn’t a cross-sectional snapshot, but a true within-person biological change after infection.
Jan 14 • 20 tweets • 3 min read
For years, Epstein–Barr virus (EBV) has been linked to multiple sclerosis.
The association was strong.
But the mechanism remained frustratingly abstract - until now.🧵
This new paper in Cell (2026) finally does what’s been missing.
It doesn’t just connect EBV and MS statistically -
it shows how the immune system gets it wrong.
Jan 13 • 18 tweets • 3 min read
People with Long COVID often describe brain fog, mental fatigue, slowed thinking.
For a long time, we lacked direct biological evidence that something measurable was wrong in the brain.
Now we have one🧵
This new study used 31P magnetic resonance spectroscopy.
Unlike standard MRI, it doesn’t look at brain structure - it looks at cellular energy metabolism.
Jan 7 • 15 tweets • 3 min read
SARS-CoV-2 leaves a mark on adaptive immunity
that resembles a mild but broad functional immunodeficiency.
Even without long COVID.🧵
A new preprint study followed the same individuals before and after SARS-CoV-2 infection and asked a simple question -
What happens to immune memory after COVID?
Not during acute illness.
Not only in long COVID.
But months later, in people considered recovered.
Jan 4 • 14 tweets • 3 min read
Prenatal COVID can shift the trajectory of brain development.
The differences are measurable - and they appear before diagnoses exist.
It’s based on neonatal brain MRI and standardized developmental testing🧵
What study is this?
A prospective study (Brain, Behavior, and Immunity, 2025)
children exposed to SARS-CoV-2 in utero
brain MRI ~2 weeks after birth
developmental testing at 2 years (Bayley-III, ITSEA)
compared to a pre-pandemic control cohort
Jan 2 • 11 tweets • 2 min read
The authors show that COVID-19 can disrupt the heart’s electrical wiring (the cardiac conduction system) -causing bradycardia, pauses, and AV block...🧵
... even when they can’t detect viral proteins in the heart, pointing instead to innate immune signaling (IFN/JAK–STAT) plus mitochondrial oxidative stress (ROS) as the likely drivers.
Jan 2 • 10 tweets • 2 min read
A new study (Cell Reports, 2026) raises an uncomfortable question.
Is metformin really immunologically neutral when used outside diabetes?
Metformin is widely discussed beyond diabetes - aging, cancer, infections, even immune modulation.🧵
It’s not just how much protein, but how proteins are chemically modified (oxidation, glycation, etc), shifting them toward pro-coagulant behavior and impaired microcirculation - and different phenotypes (Long COVID vs POTS) show different PTM signatures.
