COVID turns common EBV reactivation into a clinically significant event.
A new Czech study (Cell Reports, 2025):
SARS-CoV-2 can trigger Epstein-Barr virus (EBV) reactivation - and in some people, that leads to long-term lung damage in long COVID.🧵
The study analyzed 687 people with long COVID (4–16 weeks after infection).
Tests included:
lung function & chest X-ray
EBV serology (VCA IgM, IgA, EA-D IgG)
EBV DNA in blood
IL1/IL10 genetics
cytokines & immune profiling
Signs of recent EBV reactivation were found in 23% of patients.
Key marker: anti-VCA IgA
This antibody:
indicates a strong, recent EBV reactivation
correlates with lung damage and higher EBV viral load in blood
Reactivation was more common in people with certain genetic variants:
IL1A rs1800587 GG
IL1B rs1143634 GG
IL1RN rs315952 TT / rs579543 A
These variants increase IL-1Ra, dampen inflammation
Easier for EBV to reactivate and persist
Patients with EBV reactivation were more likely to have:
2× higher chance of abnormal chest X-rays
reduced gas exchange (DLCO, KCO)
higher latent EBV levels in blood
Often without reporting stronger symptoms!
But EBV reactivation is common, right?
Yes - even in pre-pandemic controls, it occurred in - 27%.
At first glance: COVID might not be involved.
But hold on:
The difference was not how many reactivated EBV - but how strongly and with what consequences:
Long COVID patients had much higher levels of anti-VCA IgA
This correlated with lung injury and EBV DNA in blood
COVID-19 thus modulates reactivation:
From a harmless event - to a biologically active one
Takeaway:
SARS-CoV-2 can facilitate EBV reactivation in genetically predisposed individuals
This reactivation may be “silent” - but causes measurable damage
Long COVID is not just about SARS-CoV-2 - it’s about what the virus sets off inside the host
The study was led by a team from University Hospital Olomouc & Palacký University in the Czech Republic.
It shows how viral interactions + host genetics = persistent inflammation & damage @marian_hajduch @szupraha @ZdravkoOnline cell.com/cell-reports/f…
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COVID can damage memory - even months after recovery.
Not just any memory: the precision of memory, tied to the hippocampus.
A new study shows that it doesn’t recover over time!
It actually gets worse.
A short thread on the hippocampus, neurogenesis, and a virus that lingers.🧵
The hippocampus isn’t just - a memory disk.
It’s one of the only brain areas where new neurons grow in adulthood!
It helps us:
learn new things
navigate space and time
distinguish between “same” and “similar”
Exactly what “brain fog” disrupts.
A new study (Meyer & Zaiser, 2025) tested >1400 people using a memory precision task.
People post-COVID showed significantly lower scores (LDI).
The deficit appeared even in those who felt fully recovered!
This wasn’t fatigue or depression.
It was hippocampal dysfunction.
A major new review from Yale (Moen, Baker, Iwasaki, 2025) offers the most comprehensive picture yet of what SARS-CoV-2 does to the nervous system.
The conclusion is stark:
Long COVID is a chronic neuroimmune disorder affecting brain, spinal cord, and peripheral nerves.🧵
Warning Sign #1: The pandemic didn’t end - it just changed shape.
The virus keeps evolving. The acute symptoms may fade.
But for many, the infection never truly ends.
Even young, previously healthy people experience:
mental fog,
dizziness when standing,
sensory disturbances,
exhaustion after minimal effort,
racing heart.
That’s Long COVID.
Warning Sign #2: The virus leaves behind molecular debris - and the immune system won’t let it go.
Sometimes it’s spike protein fragments in the blood.
Sometimes viral RNA in the olfactory bulb or even the skull.
This triggers persistent immune alarms:
T cells get activated
Inflammation spreads to the brain
Neuronal connections start breaking down
The war continues - long after the virus is gone.
A new 2025 preprint confirms: Long COVID (PCS) is biologically real - and it’s in the brain.
The key culprit? Chronic, low-grade neuroinflammation.
It can persist for months or even years.
Here why it matters 👇
What is PCS (Post-COVID Syndrome)?
Not “just anxiety.
Not “just fatigue.”
It’s a state of ongoing immune activity in the brain after SARS-CoV-2 infection!
Common symptoms:
brain fog
fatigue
anxiety
sleep disturbances
memory loss
What drives brain inflammation?
This study identifies 9 key mechanisms keeping it alive:
spike protein persisting in brain/skull
chronic glial activation
blood-brain barrier (BBB) disruption
autoimmunity
viral reactivation (EBV, HERVs)
microclots & hypoxia
vagus nerve dysregulation
mast cell activation
histamine system abnormalities
What connects HIV and SARS-CoV-2 in the brain?
Not structural homology - but functional parallels between viral proteins that can drive chronic neuroinflammation and immune evasion.
A short thread on Tat, viroporins, ORF8, and viral neuropathogenesis. @dbdugger 🧵
COVID-19 (Long COVID) is associated with:
microglial activation
blood-brain barrier (BBB) disruption
persistent viral antigens
memory and attention deficits
These are also key features of HIV-associated neurocognitive disorder (HAND). What’s the link?
In HIV, the Tat protein is central to neuropathology:
secreted from infected cells
crosses the BBB
activates microglia via TLR4
triggers IL-6, TNFa, ROS
promotes excitotoxicity in neurons
Tat = neurotoxic transcriptional regulator.
In recent months, a growing number of robust scientific studies have confirmed that even mild SARS-CoV-2 infection is not biologically neutral in children. Two new studies reveal surprising depth of impact - metabolically and immunologically.🧵
For years, pediatric COVID-19 was framed as "mild."
But a large metabolomic study (Lawler et al., 2025) shows that even children with mild symptoms show significant systemic changes in their blood - and a newer study (Gaebler et al., 2025) suggests some of these changes persist.
Lawler et al. analyzed 147 children
55 had acute COVID-19 (most were not severely ill)
What if time really started ticking faster after COVID?
Renner et al. (2025) and a new @PolyBioResearch - supported study both show:
Post-COVID immune activation may silently age the body, damage organs, and reduce resilience.
Let’s connect the dots.
@dbdugger @RealCheckMarker @1goodtern
Renner et al. (2025) studied 68 patients with Long COVID.
Most of those with moderate/severe symptoms showed:
Persistent CD8+ T cell activation
Loss of naive T cells
High IL-3 (a hematopoietic inflammatory signal)
It’s immune rewiring. sciencedirect.com/science/articl…
These immune changes correlate with gradual damage to ACE2-rich organs (drug-metabolizing):
Kidneys
Liver
That means potential trouble for:
Blood pressure meds (ACEi/ARBs)
Antidepressants, hormones, NSAIDs
Vaccines
Metformin
Even paracetamol...