Rather than framing long COVID as a simple state of persistent systemic inflammation, this new study points toward a model of chronically dysregulated immunity in which NK-cell dysfunction may occupy a central mechanistic role🧵

https://twitter.com/harryspoelstra/status/2030951652866371967

This paper says something important. In at least a subset of patients, long COVID may represent a state of impaired, inefficient, and partly exhausted immune surveillance, with NK cells at its center.

A new PET study in patients with treatment-resistant depression suggests something important - ketamine does not just act generally on glutamate - it appears to reshape AMPA receptor density in specific brain circuits. @DavidJoffe64 🧵 The researchers used [11C]K-2, a tracer that can visualize AMPA receptors in the living human brain.
That matters because AMPA receptors are a key part of glutamatergic signaling.

A new preprint proposes an interesting mechanism for Long COVID - a link between gut dysbiosis - microbial extracellular vesicles - systemic inflammation - neuroinflammation.
This is not just correlation. The authors also test functional models.🧵 The main idea - after SARS-CoV-2 infection, patients may develop a persistent alteration of the gut microbiome. This does not only mean a different bacterial composition, but also the production of different signaling particles - so-called gut microbiota-derived extracellular vesicles (GMEVs).

A new study looked at long-term taste dysfunction after COVID-19.
Researchers combined psychophysical taste tests, biopsies of tongue papillae, and gene-expression analysis in taste cells from patients with persistent symptoms more than a year after infection🧵 One striking observation - in most patients, taste buds were not structurally destroyed. Under the microscope, both taste receptor cells and the nerve fibers that normally innervate them were still present.

A very interesting 2026 study compares classic ME/CFS, post-COVID ME/CFS like (PCS-CFS), and MS.
It doesn’t just measure antibodies - it tests their functional effects on cells (in vitro).
And the takeaway? Post-COVID does not look identical🧵 Researchers isolated IgG antibodies from patients and exposed endothelial cells to them.
They analyzed mitochondrial structure, cellular energetics, inflammatory cytokines, immune complex proteomics
This allows biological comparison across groups.

Two recent studies suggest that Long COVID may involve long-term neurobiological remodeling - even after mild infection.
One examined the brain under cognitive load.
The other looked at it at rest.
Together, they point to a persistent shift in network organization!🧵

https://twitter.com/zdenekvrozina/status/2023188837309227210

In the first study (Barnden et al.), the key issue was not where the brain activates -
but how its networks coordinate under mental exertion.
The largest differences appeared during cognitive load.
The regulatory switching system began to fail.

In this group of people who self-identified as having Long COVID and were willing to complete an online survey, Long COVID is very long-lasting - around 20 months after symptom onset, only about 5% were fully back to baseline.🧵 The median duration of symptoms was about 20 months.
Only 5% of patients fully recovered.
About 59% never had a symptom-free day.

This paper is a systematic review summarizing 10 studies focused on cardiovascular findings after COVID.
The main message is - Long COVID is associated with measurable changes in the heart and blood vessels🧵

https://twitter.com/BagaiDr/status/2028036581001691253

Systematic review according to PRISMA 2020
PubMed, Scopus, Web of Science
1/2020 - 3/2024 (updated 11/2025)
Out of 412 records, 10 high-quality studies were selected.

When we talk about COVID in children, we often hear - mild disease.
The real question we rarely ask is this - what if some children leave the infection with a silent, measurable cardiovascular footprint - and we simply don’t have long enough follow-up yet to see what it leads to?🧵 About a quarter of children.
In a new study, 16 out of 67 kids (24%) had subclinical cardiac contractility changes three months after mild or asymptomatic COVID - despite having no persistent symptoms.

The interesting proof-of-concept study shows that in some severely immunocompromised people with long-lasting COVID-19, it is possible to use autologous VSTs🧵 It is possible to -
Produce SARS-CoV-2–specific T cells from their own blood (autologous VSTs),
Infuse them back into the patient,
In the 3 treated patients this was temporally associated with clinical improvement, PCR turning negative, and better CT findings - without serious side effects.

One overlooked signal of the pandemic. IL-32 - a cytokine known from HIV research as a marker of chronic immune activation - is now elevated not only in COVID patients, but across large parts of the general population🧵

https://twitter.com/zdenekvrozina/status/2026037007873413219

Here’s an underappreciated detail. IL-32 isn’t just another inflammatory cytokine. In HIV research, it’s a well-known marker of chronic immune activation - linked to persistent low-grade inflammation and long-term viral persistence

When the precautionary principle is not applied to pregnancy and brain development, it fails its purpose.
An informed framework and systematic follow-up should have come earlier - and are still needed🧵 One more study in a long line of findings adds hard endpoints
neonatal brain MRI
standardized developmental testing at age 2.

SARS-CoV-2 may leave a long-lasting population imprint - not a dramatic cytokine storm, but a quiet, low-grade, atypically regulated inflammatory background. One measurable signal of this may be the cytokine IL-32🧵 In a new study of 1,000 healthy blood donors and 212 hospitalized COVID-19 patients, researchers found IL-32 levels were significantly higher not only in severe cases, but across the general population during the pandemic.

New study in Nature Aging.
Metformin slows inflammatory aging through a completely unexpected mechanism.
This isn’t just about metabolism.
It’s about misplaced DNA.🧵

https://twitter.com/agingdoc1/status/2025398639049244948

In aging and senescent cells, fragments of chromatin can break off and leak into the cytoplasm.
These are called cytoplasmic chromatin fragments (CCFs) - essentially pieces of our own DNA in the wrong place.

COVID as a neurovascular brain problem. A new study shows impaired regulation of cerebral blood flow during mental exertion.
In patients with long COVID, this finding was associated with worse cognitive performance🧵

https://twitter.com/DavidJoffe64/status/2025443443032649853

Important context - long COVID patients were assessed at an average of ~314 days after infection (10 months).
The study did not specify the viral variant, but based on timing, some infections may have occurred during the Omicron era.

This pediatric long COVID study found an immune fingerprint where the authors explicitly flag parallels with chronic viral infections (they name HIV-1) not as a slogan, but as part of how they interpret their own data🧵

https://twitter.com/harryspoelstra/status/2024783160949481802

JCI Insight 2026. Pediatric long COVID vs kids post-infection without long COVID, sampled around ~3 months after acute infection.
We covered this topic in the preprint, now we’re going into more detail given how important it is.

After COVID and HIV (even on ART), your cells can carry a clear immune aging signature - especially inside naive CD8 T cells🧵 A new paper uses single-cell RNA-seq to ask a sharper question.
Is the aging signal coming from changed immune-cell proportions (systemic), or from aging-like shifts inside the cells themselves (intrinsic)?

SARS-CoV-2 in brain tumors - what does it actually mean?
A new study analyzed brain tumor samples from 72 COVID-19 patients (Omicron BA.5 wave) to see whether the virus can be found directly inside tumors - and how it affects their immune environment🧵

https://twitter.com/harryspoelstra/status/2024480055053697157

First - nothing mystical here.
Tumors are still tissue. They often have abnormal vessels, disrupted barriers, and altered immunity.
So the real question isn’t can virus be there? - but what happens if it is.

Even three years post-infection, a subset of COVID survivors shows a persistently altered immune landscape, marked by elevated cytokines and incomplete recovery of key immune cell populations.🧵

https://twitter.com/vipintukur/status/2024483716563947953

Some inflammatory signals remain elevated, and certain immune cell populations never normalize. The strongest and most consistent changes involve the T-cell compartment rather than innate immune cells.

This new study shows that SARS-CoV-2 can systematically reprogram cellular metabolism to support its own survival.
This isn’t just tissue damage.
It’s a redirection of the body’s energy systems🧵

https://twitter.com/atranscendedman/status/2023447719281627194

This is a recent mini-review examining how COVID-19 affects lipid profiles and the metabolome, especially in people with type 2 diabetes.
By synthesizing multiple studies, the authors show that SARS-CoV-2 profoundly disrupts metabolic balance.

Researchers looked at markers of cellular and mitochondrial damage in the blood of people with Long COVID and linked them to cognition, psychological distress, and inflammation. They identified several surprising associations🧵 Finding 1. Long COVID = lower relative ccf-mtDNA
At first glance, this is surprising.
People usually expect - mitochondrial damage - more mtDNA released into blood.
But here, researchers found lower relative levels.