Severe COVID-19 leaves behind a long-lasting, systemic, and biologically measurable pro-oncogenic state
that persists for at least one year after infection and may increase cancer risk or worsen cancer prognosis🧵
The authors analyzed long-term changes in gene expression in peripheral blood mononuclear cells (PBMCs) one year after COVID-19 infection.
Dec 13 • 22 tweets • 3 min read
COVID-19 is not just an acute event - it is a long-term vascular insult.
This study shows that the risk of ischemic stroke remains elevated for at least four years after SARS-CoV-2 infection.🧵
The risk remains elevated including in people who
were not hospitalized,
had a mild or moderate course,
had no obvious neurological complications during the acute phase.
Dec 12 • 21 tweets • 3 min read
What a new Nature Immunology study shows about long COVID?
Long COVID is not post-infectious fatigue.
A new study shows that it is a clearly defined biological state =
chronic immune activation, T-cell exhaustion, and metabolic disruption🧵
The study analyzed 142 individuals, including 28 patients with long COVID.
Compared with recovered controls, people with long COVID showed persistent activation of inflammatory pathways lasting more than 180 days after infection.
Dec 12 • 20 tweets • 3 min read
Can pathological processes continue in the brain without an active virus?
Yes.
The SARS-CoV-2 nucleocapsid (N) protein on its own can accelerate microglial aging by switching cellular metabolism toward glycolysis, leading to measurable memory impairment🧵
This study shows that the N protein is not biologically neutral.
Even in the absence of viral replication, it is sufficient to trigger long-lasting dysfunction in the brain.
Dec 9 • 14 tweets • 2 min read
COVID isn’t only about the virus being strong - but about the body’s ability to restore balance being disrupted. So a another direction is emerging -
instead of only studying what the virus does, researchers are looking at how the body’s regulatory systems break down🧵
A recent review shows that SARS-CoV-2 can block the cell’s clean-up system, which normally removes damaged molecules and leftover virus. When this system stalls, viral pieces remain, the immune system stays activated, and inflammation escalates.
Dec 7 • 15 tweets • 2 min read
A new study mapped how SARS-CoV-2 variants disrupt human biology using a custom tool called BioEnrichPy.
Unlike typical pipelines, it automates the full workflow - data parsing, enrichment (GO/KEGG), stats, visual output🧵
Why this matters.
Variant-specific host interactions are usually analyzed manually - slow, fragmented, and error-prone.
BioEnrichPy standardizes this into a reproducible, scalable process that can handle large interactomes.
Dec 6 • 18 tweets • 3 min read
A large peer-review study from China (40,537 people, 3 hospitals, 2021–2024) found that a single wave of SARS-CoV-2 infection (Omicron BA.5/BF.7) was followed by a measurable loss of T cells that lasted more than 20 months.
Not a small fluctuation - a durable shift in immunity.🧵
Study headline result.
~10% reduction in CD8+ T cells still present ~20 months after infection.
For an individual - maybe subtle.
For a population -a meaningful shift in antiviral capacity.
Dec 4 • 13 tweets • 3 min read
A large new study published in JAMA Network Open examined 28 million adults in France (ages 18–59) over four years to assess the long-term risk of death after mRNA COVID-19 vaccination🧵
The bottom line - vaccinated individuals had about 25% lower risk of overall death (all-cause mortality) compared with people who never got vaccinated.
Dec 4 • 19 tweets • 3 min read
A new review by Miller, @VirusesImmunity at al. appeared in Trends in Immunology.
This isn’t a clinical guideline or treatment plan.
It’s a historical-immunological framework summarizing what we know about Long COVID - and especially what this knowledge implies🧵
Long COVID is far from rare. With an estimated 10% prevalence, it represents a real population-level burden.
Symptoms are varied and span many organ systems.
Long COVID is not one syndrome, but a collection of biological phenotypes, from cognitive dysfunction to microvascular and immunologic issues.
Dec 4 • 15 tweets • 2 min read
A new meta-analysis (28 cohort studies, 1 billion participants) finds that SARS-CoV-2 infection is associated with a 40% increased risk of developing new mental disorders compared with non-infected individuals.
Risk difference? +31 cases per 1000 people🧵
The strongest associations were seen for neurocognitive disorders, mood disorders, and anxiety disorders. COVID-19 survivors were also 74% more likely to be prescribed psychotropic medications after infection!
It’s measurable clinical disease.
Dec 2 • 18 tweets • 3 min read
A new study from Germany looked at the eyes of people who recovered from COVID-19, even months later.
Using a non-invasive retinal imaging tool (OCTA), they found signs of microvascular injury - even in people who had only mild illness.
And it links to long COVID fatigue🧵
COVID-19 leaves microvascular damage, even after mild infection
People who had COVID-19 showed a larger foveal avascular zone (FAZ) - basically a patch in the retina where tiny capillaries are missing.
This was most pronounced in patients who were not hospitalized.
Dec 1 • 16 tweets • 3 min read
A study comparing the immune system 3 months after COVID-19 and after influenza shows something clear.
SARS-CoV-2 leaves behind a far deeper and longer-lasting immune imprint than seasonal flu.
And the difference isn’t subtle🧵
Researchers used high-dimensional 40-marker CyTOF to map dozens of immune cell types in detail.
The result was so distinct that machine-learning models could accurately classify post-COVID vs post-flu individuals (AUC > 0.95).
Dec 1 • 12 tweets • 2 min read
A new observational study examined whether metformin prescribed within the first week of SARS-CoV-2 infection reduces the risk of Long COVID - what it actually shows🧵
The authors used N3C electronic health records and a target trial emulation design to compare metformin vs several other COVID-related prescriptions.
Nov 30 • 20 tweets • 4 min read
A new review breaks down what SARS-CoV-2 ORF/accessory proteins actually do - from interferon suppression to mitochondrial disruption. Here are the key points, followed by how some of these mechanisms compare to those used by HIV🧵
A new review makes something very clear.
SARS-CoV-2 doesn’t rely only on spike. It uses a broad arsenal of accessory proteins (APs) that shape
how severe the acute phase becomes,
which organs are affected,
and the biological conditions that make long-term sequelae more likely.
These proteins aren’t side notes - they’re central modules of pathogenesis.
Nov 29 • 16 tweets • 3 min read
Cognitive PASC (COVID brain fog with measurable cognitive decline) isn’t just another flavor of long COVID.
This new important study shows its a biologically distinct condition that carries features resembling early neurodegenerative processes - even after mild COVID🧵
Evidence of brain injury in cognitive PASC -
The cognitive PASC group shows clear signs of astroglial injury
elevated GFAP (astrocyte damage marker)
NfL not elevated, meaning no widespread axonal destruction
This suggests a chronic, low-grade neuroinflammatory–degenerative stress.
Nov 29 • 18 tweets • 3 min read
COVID can cause a long-lasting breakdown of immune homeostasis, where elevated IL-7 and IL-15 keep T cells activated for months after the acute infection.
In some people this dysregulated state becomes persistent - and may directly contribute to long COVID🧵
This is an important shift in understanding. It’s not just that T cells stay activated - the key question is why.
The new study shows that the drivers are homeostatic cytokines that normally help rebuild the T-cell pool after infection.
Nov 28 • 21 tweets • 4 min read
SARS-CoV-2 causes long-lasting structural changes in the brain - even in people without symptoms.
Recovered ≠ normal. In this study, every single recovered participant still showed measurable abnormalities.
And this is 6-12 months after infection🧵
47 participants - Long COVID (19), recovered without symptoms (12), uninfected controls (16)
Multimodal 3T MRI - myelin (T1w/T2w), white matter microstructure (MD/AD/RD/FA), MR spectroscopy
Variant based on timing/location - Australia 2022–23, this was almost certainly Omicron
Headline?
Both post-COVID groups show clear structural brain differences.
Nov 27 • 15 tweets • 2 min read
SARS-CoV-2 spike can trigger Sjögren-like damage in salivary glands - and the parallels with HIV are striking.
Salivary glands are not passive tissue. They’re immune active organs with TLR2/4, resident lymphocytes, and epithelial cells that behave like mini immune sensors🧵
A new study shows something interesting. The SARS-CoV-2 spike protein alone - without virus, without ACE2 entry - can cause significant damage to submandibular glands, closely resembling early Sjögren’s disease.
Nov 26 • 20 tweets • 3 min read
A new 3-year scRNA-seq study shows something striking. Some people after COVID still carry an immune profile that looks like accelerated aging - low naive T cells and persistent activation of pathogenic Th17. Not a long-COVID cohort, but biologically very close🧵
The study didn’t select people with long COVID.
It followed 47 individuals after COVID-19 for 3 years - and some symptoms were reported within the cohort, allowing the authors to examine symptom-associated immune signals without defining a long-COVID subgroup.
Nov 24 • 19 tweets • 3 min read
When we look at the brain after COVID, we need to accept something that still hasn’t fully landed in public understanding - changes in cerebral perfusion aren’t limited to people with Long COVID. They show up in almost everyone.
And this new study makes that point clear🧵
What the authors demonstrate is simple but essential - the perfusion changes they found aren’t exclusive to PCC patients - they also appear in the controls, who had COVID but don’t report chronic symptoms.
Nov 22 • 21 tweets • 3 min read
This study shows something striking.
The spike protein by itself can trigger ACE2-targeted autoimmunity - causing lung and kidney injury without any viral infection.
This may help explain why COVID-19 can damage organs even when no virus is detectable in the tissue🧵
Researchers immunized Wistar rats with recombinant SARS-CoV-2 spike protein.
Control animals received the same adjuvant (IFA).
The only difference was the spike antigen itself.
