This study brings direct evidence that replication-competent SARS-CoV-2 can persist in the brainstem of living mammals for at least 80 days after infection!
A major milestone in understanding the biology of long COVID.🧵
Researchers infected golden hamsters with Wuhan, Delta, and Omicron/BA.1 variants.
On day 80 - long after symptoms were gone - they sampled the brainstem.
In most animals, they isolated live, infectious virus capable of replication in cell culture.
This means the brainstem can act as a viral reservoir - even after the virus clears from the lungs.
That challenges the idea that long COVID is just residual inflammation.
Instead, it points to ongoing infection in specific tissues.
What does that do to the brain?
They found
disrupted dopaminergic and glutamatergic signaling,
gene signatures linked to neurodegeneration (eg mitochondrial dysfunction, impaired proteostasis),
altered expression of genes tied to Alzheimer’s and Parkinson’s.
Behaviorally, these animals developed:
memory problems,
anxiety-like symptoms,
depressive behaviors (in females especially).
No stress, no social context - just the biological effects of the virus.
The authors’ key message:
SARS-CoV-2 leaves behind a neurodegenerative-like molecular footprint in the brainstem.
That signature persists long after acute infection - and may explain long COVID symptoms like brain fog, fatigue, and mood disorders.
What connects the lungs and blood vessels two years after COVID-19?
A new Brazilian study followed patients with persistent symptoms more than two years post-infection. What they found was striking: measurable damage in both lungs and vessels – and a clear link between the two.🧵
The study looked at 32 individuals with long COVID symptoms, about 32 months after their initial infection.
They tested:
Lung function (FEV1/FVC, KCO)
Endothelial function (via flow-mediated dilation - FMD)
Post-COVID functional status (PCFS scale)
One of the clearest findings? Even two years after infection, vascular function was still abnormal.
On average, participants had FMD of –0.21% - while healthy values are typically above 5%.
A negative FMD means the blood vessels narrowed in response to flow, instead of dilating - a strong signal of endothelial dysfunction.
Late but finally.
Top researchers (NIH, Yale, Karolinska, UCSF…) are now calling for a shift in how we run acute COVID-19 trials:
We must start measuring viral persistence as a biological outcome - even during the initial infection phase🧵
The logic draws from decades of experience with HIV, HCV, and precision oncology:
Chronic viral reservoirs are real
They’re hard to detect
And they require tailored, often combined therapies to target
Sound familiar?
In long COVID, viral RNA and proteins have been found in tissues (gut, brain), immune cells, and circulating plasma months after infection.
At the same time:
persistent spike antigenemia
exhausted virus-specific T cells
low-level inflammatory signatures
All pointing to a lingering reservoir.
ASHRAE 241: What to do when a virus spreads through the air.
This standard defines how much clean air per person is needed to reduce infection risk - but only during outbreaks.
It doesn’t apply all the time.
Here’s what it says and why it matter🧵
ASHRAE 241-2023 was created for times when viruses are spreading in the community.
It activates a special mode called IRMM - Infection Risk Management Mode.
That means
This is for outbreaks, not everyday conditions.
The goal is clear:
Reduce airborne transmission in indoor spaces during periods of higher risk.
It doesn’t cover short-range droplets or surfaces - just the risk of getting infected by sharing air in a room.
Viruses like HIV and CMV don’t just evade immunity - they reshape the host from within.
One way they do it? By targeting the cell’s ability to make proteins.
SARS-CoV-2 belongs in this group. It interferes with how ribosomes are made and used.
What that means - and why it matters 🧵
Viruses like HIV are known to:
block protein translation
rewire cell signaling
change cellular behavior without altering DNA
SARS-CoV-2 does the same.
Its Nsp1 protein hijacks ribosomes - the core machinery that turns RNA into protein.
Ribosomes are molecular machines that translate genetic instructions (mRNA) into proteins.
Without them, a cell can’t repair itself, send immune signals, respond to stress or survive infection.
This new Nature Immunology study is wild.
Turns out, CD8+T cells can go into an exhausted-like state without any chronic infection.
No persistent virus. No repeated antigen.
Just broken mitochondria.
Complex III.🧵
Quick recap: Complex III is part of the mitochondrial electron transport chain.
It pumps protons (ATP), passes electrons (metabolism), and makes ROS (signaling).
The authors knocked it out in T cells. What happened?
The T cells couldn’t divide, couldn’t form memory, and looked dysfunctional.
Then they added AOX - a sea squirt enzyme that restores electron flow without making ROS or pumping protons.
So: respiration back, but no ROS, no ATP from Complex III.
SARS-CoV-2 targets mitochondria. That’s not collateral damage - that’s a strategy.
A July 2025 review in Redox Biology brings together striking evidence of viral mitochondriopathy in COVID-19 and Long COVID.🧵
It shows how SARS-CoV-2 reprograms host cells by attacking their energetic and immunologic core: the mitochondria.
Here’s what that means:
What the virus does to mitochondria:
Inhibits oxidative phosphorylation (OXPHOS) = less ATP
Increases ROS and triggers mitochondrial DNA (mtDNA) release
Disrupts MAVS - the antiviral signaling hub
Switches metabolism to aerobic glycolysis (Warburg effect)
Blocks mitophagy = damaged mitochondria accumulate
Triggers pyroptosis, apoptosis & DAMP release