Two 2025 studies confirm it:
In some people, COVID leaves parts of the brain functionally switched off.
PET and EEG both show disruptions in regions that control attention, motivation, and emotion.
What that actually means🧵
Reduced glucose metabolism = less energy in certain parts of the brain, measured with PET using radioactive glucose. Siqueira et al., 2025.
Most affected: the left orbitofrontal cortex (just above the eyes), often extending into the frontal lobe.
This brain region handles:
executive functions
attention
emotional regulation
motivation
social behavior
When it’s underpowered - you may feel
brain fog
anxiety or apathy
lack of drive or disconnection from others
Clinically, this matches what long COVID patients often describe:
I know what I want to do, but I just can’t get it done.
Everything takes me forever. I can’t think straight.
I don’t feel like myself.
These aren’t vague complaints. They point to a real biological disruption.
EEG slowing - brainwaves shifting to a slower rhythm. Manganotti et al. 2025
What it is:
More slow waves (delta, theta)
Fewer normal rhythms (alpha, beta)
Where: Mostly in the left frontal region - the same area affected on PET
What it means:
EEG slowing is a non-specific but serious sign of cortical dysfunction.
You see similar EEG patterns in
Alzheimer’s
inflammatory encephalopathies
severe metabolic disorders
In plain terms: this means the brain in these regions isn’t processing information effectively.
Why does it matter that PET and EEG show the same thing?
Two completely different tools (metabolism vs. electrical activity)
pointing to the same disrupted area
in the same group of patients
That’s strong evidence.
Not random.
Not just patient perception.
It’s an objective, biological problem.
How does this fit into the long COVID puzzle?
SARS-CoV-2 affects:
blood vessels in the brain
inflammation and microglial activation
the blood–brain barrier
These can all lead to localized metabolic dysfunction in brain tissue.
And when both low metabolism and disrupted brain rhythms persist for months…
certain circuits stay dimmed
which explains chronic symptoms we associate with long COVID
This isn’t just tiredness or stress.
It’s measurable dysfunction.
Persistent hypometabolism and EEG slowing have also been observed after:
HIV
HSV-1 encephalitis
Influenza A in severe cases
Zika virus, especially in infants
SARS-CoV-2 appears to join this group - but uniquely affects the orbitofrontal cortex more often and can do so without causing classic encephalitis.
The brain remembers. And sometimes, COVID doesn’t just fade away.
So if you’re experiencing brain fog after COVID - it’s not just in your head.
PET and EEG show clear signs of disrupted function, especially in brain areas critical for daily life.
Manganotti et al. 2025. Mapping brain changes in post-COVID-19 cognitive decline via FDG PET hypometabolism and EEG slowing. nature.com/articles/s4159…
Siqueira et al., 2025. Metabolic brain changes in post-acute COVID-19: systematic review and meta-analysis of [18F]-FDG-PET findings. link.springer.com/article/10.100…
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More than 2 years after infection, people with Long COVID still show signs of a leaky blood-brain barrier (BBB) - the brain’s protective filter.
A new MRI study links this persistent leakiness to motor dysfunction. Here’s what that means🧵
The BBB acts like a security checkpoint for the brain.
It keeps out toxins, viruses, immune cells - anything that could harm sensitive brain tissue.
When the barrier breaks down, the brain becomes exposed to inflammation, immune attacks, and possibly long-term damage.
This study used a noninvasive MRI technique - WEPCAST.
It tracks how easily water - a tiny molecule - crosses the BBB. That makes it more sensitive than standard MRI with contrast or spinal taps.
High precision.
Metformin cut the risk of long COVID.
A randomized, placebo-controlled trial tested a short course of metformin given during acute COVID.
While the primary endpoint didn’t reach the pre-specified threshold, some secondary outcomes were striking🧵
COVID-19 in early childhood disrupts the gut microbiome - even without symptoms - and may dampen key immune pathways. A new study sheds light on this underappreciated risk. Let’s break it down🧵
Researchers studied children under 2 years old with mild COVID-19.
No GI symptoms!
Still, their gut microbiome looked very different from healthy peers.
Less diversity
Loss of protective bacteria
Rise in opportunistic bugs
Predicted suppression of immune-related pathways
Why does this matter?
Because early childhood is when the immune system learns - and the gut microbiome is the teacher.
Disrupt the microbial community, and you risk shaping immune responses in unhealthy ways.
A big US study (HEROS, 1156 people, May 2020-Feb 2021) found something surprising.
If you had a rhinovirus (common cold) in the past month, your chance of catching COVID was 48% lower.
If you still got it, your viral load was almost 10× lower.🧵
Why?
Rhinovirus flips on a powerful interferon alarm in your airway cells.
Result - 24 antiviral genes (RIG-I, MDA5, IFIT1…) are primed and ready to slow down other viruses - including SARS-CoV-2.
The effect is instant:
These genes fire right in the airway epithelium, so the defense starts before immune cells even arrive.
Long COVID & viral persistence - new evidence
A new study detected a peptide fragment specific to SARS-CoV-2 nsp3 in blood extracellular vesicles (EVs) from Long COVID patients - months to years after infection.
Let’s unpack why this matters.🧵
EVs are tiny membrane packages released by cells, carrying proteins, RNA, and lipids.
They can travel in blood, cross biological barriers, and deliver their contents to other cells - bypassing normal immune surveillance!
The detected peptide - GSLPINVIVFDGK - is uniquely part of nsp3, a large viral enzyme encoded by ORF1ab.
Nsp3 is crucial for SARS-CoV-2 replication and immune evasion.
Importantly - the study found the peptide, not necessarily the entire intact protein.
Even without live virus, blood serum can carry signals powerful enough to change how healthy tissue works.
A new peer-reviewed study shows serum from ME/CFS and long COVID patients can directly impair muscle function in lab-grown human muscle.
5 years in, we still don’t know exactly which factors are responsible 🧵
The team built sophisticated 3D mini-muscles from human myoblasts. These bioengineered tissues contract when electrically stimulated, much like real muscles.
Then they bathed them in serum from ME/CFS or long COVID patients and watched what happened.
The results were striking.
After just 48 hours, previously healthy muscle tissue showed:
weaker contractions,
shorter endurance,
disrupted calcium (Ca2+) regulation,
clear signs of mitochondrial stress.
In short - muscles that were working perfectly started behaving like diseased ones.