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🧵

https://twitter.com/HarrySpoelstra/status/1992172984996442286

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.

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.

This new Nature Communications study is the most comprehensive look we’ve ever had at SARS-CoV-2 inside the human fetus.
And the message is straightforward.
Vertical transmission is real,
and the virus can reach multiple fetal organs - even early in pregnancy🧵 For years we heard that fetal infection was rare.
But that was based on limited testing, often using low-sensitivity methods.

A new review pulls the whole picture together. SARS-CoV-2 doesn’t just infect. It disrupts immunity at multiple levels - from interferons to inflammasomes to deep T-cell exhaustion.
If you still think COVID is just a respiratory virus, this paper will change your mind🧵. @DavidJoffe64 The study shows why severe COVID and Long COVID share the same roots - mis-timed immunity, destructive inflammation, and exhausted T cells that struggle to clear antigen or build lasting protection.
It’s now well-documented.

Three years after infection, the virus still leaves a fingerprint. The damage is clear - profound mitochondrial dysfunction in CD56bright NK and CD4 T cells - a problem that only appears when the immune system is pushed to respond.🧵

https://twitter.com/evelio_prieto/status/1991228180275859836

This study makes one thing very clear.
Long COVID isn’t just a cluster of lingering symptoms - it reflects a measurable biological state, marked by weakened antiviral immunity and impaired cellular energy metabolism

This study does more than show that SARS-CoV-2 can enter neurons. It reveals a specific and biologically meaningful mechanism by which the virus can damage the exact brain cells whose degeneration leads to Parkinson’s disease🧵 The virus doesn’t infect neurons randomly - it targets A9 dopaminergic neurons.
These are the neurons in the substantia nigra that die first and fastest in Parkinson’s disease.

A new metabolomic study does something important. It looks directly at the biochemical products circulating in plasma - a real-time readout of how cells are functioning. And the results are clear - even clinically recovered individuals show measurable metabolic and proteomic deviations from uninfected controls.🧵

https://x.com/ZdenekVrozina/status/1990374687205933522

The main finding is unmistakable. A systemic collapse of mitochondrial energy metabolism. TCA cycle intermediates down, NAD cycling disrupted, oxidative phosphorylation impaired. These biochemical changes map onto the symptoms frequently reported in long COVID (fatigue, PEM, cognitive dysfunction).

New data shows that 3-4 years after infection, people still carry highly cytotoxic spike-specific CD4+ T cells - the kind of long-lasting elite clones usually seen in persistent infections like CMV or HIV🧵 This isn’t a typical post respiratory virus immune profile.
And it tells us something important - the immune system has been pushed into a long-term, selective state that goes far beyond what we expect from an acute infection.

A new study may finally explain how EBV triggers and worsen lupus.
A paper in Science Translational Medicine + Stanford Medicine report just clarified a question researchers have chased for decades.
How can a virus that almost everyone carries ignite lupus in some people?🧵 Lupus (SLE) doesn’t just appear.
You need the right (or wrong) genetics, a breakdown in immune control, and a trigger.
This new study points to Epstein–Barr virus (EBV) as that trigger - possibly in most lupus cases.

A new study shows how the SARS-CoV-2 spike protein (S1) alone can trigger Alzheimer- and Parkinson-like processes in the brain - and how metformin can reverse them.
This isn’t a new story, but now we see the mechanism in action🧵 Lee in PLOS One demonstrate that the intranasal administration of spike protein’s S1 subunit can drive HIF-1α-mediated synaptic suppression and p-tau/α-synuclein aggregation in the hippocampus - key features of neurodegeneration.
And metformin reversed it.

A new 5-year study from Brazil shows that surviving COVID-19 can significantly alter the natural course of Alzheimer’s disease (AD).🧵 Patients who had COVID-19 were nearly five times more likely to experience rapid cognitive decline (measured by MMSE).
Their memory, orientation, and mental abilities worsened faster than expected for typical AD progression.

A interesting paper in Nature Structural & Molecular Biology finally reveals how metformin really works inside mitochondria.
It doesn’t shut down energy - it fine-tunes the flow of electrons through complex I🧵

https://twitter.com/atranscendedman/status/1987866218838049084

Complex I is the engine of the respiratory chain.
It transfers electrons from NADH to coenzyme Q10 (ubiquinone) and pumps protons across the membrane to make ATP - the cell’s energy currency.

What if SARS-CoV-2 doesn’t just infect - but also self-assembles into molecular structures that keep the immune system burning?
Zhang showed that after the virus breaks apart, some of its fragments re-form peptide-RNA nanocrystals that potently activate TLR3, even without live virus - a “viral afterlife.”🧵

https://x.com/ZdenekVrozina/status/1986978184525701301

Let’s start with what we actually know.
Zhang showed that some of SARS protein fragments can self-assemble with RNA into nanocrystalline structures that strongly activate the immune receptor TLR3 - even without live virus

Long COVID in women and men are not the same disease. They share symptoms, but diverge in biology - immune, hormonal, and genetic.
After months since the preprint -
peer-reviewed study is now out in Cell Reports Medicine.🧵 This is the complete analysis immunity, hormones, and gene expression in 78 Long COVID with ME-CFS patients.
It confirms what patients have said for years -
this condition is biological, measurable, and deeply sex-specific.

Getting the COVID and flu shot together?
A new Italian study in Cytokine found that the early inflammatory response after getting COVID-19 and flu vaccines at the same time may actually limit how long your antibody protection lasts🧵

https://twitter.com/harryspoelstra/status/1986725315356352755

29 healthcare workers received both
an mRNA COVID-19 (XBB.1.5) booster
a quadrivalent inactivated flu shot.
Blood was collected
before vaccination (T0)
5 days later (T1)
after 3 months (T2)
after 6 months (T3)

A new study from Hong Kong Baptist University examined how mRNA COVID-19 vaccines might influence insulin signaling.
The finding?
The spike protein can interfere with metabolic pathways - but mainly in people with type 2 diabetes (T2D)🧵 In mice given 4 doses of the mRNA vaccine, researchers observed impaired glucose tolerance, reduced insulin sensitivity, and higher triglycerides.

A new study in The Lancet Child & Adolescent Health followed nearly 14 million children in England.
It shows that SARS-CoV-2 infection leaves long-term marks on the vascular and immune system - even in kids.
Not just for weeks, but measurable up to a year later🧵

https://twitter.com/yash25571056/status/1986027562435289208

After COVID-19, children had a sharply increased risk of
systemic inflammatory syndromes (MIS-C, etc)
venous thrombosis
thrombocytopenia
myocarditis and pericarditis
And part of these risks remained elevated 12 months post-infection.

New study in BMC Immunology shows that COVID-19 leaves a lasting “aka Long Covid” imprint in the immune cells of older adults. What does that mean - and why does it matter?🧵 Months after recovery, immune cells in elderly people remain abnormally prone to die - through apoptosis.
Even when the virus is long gone, the immune system still shows signs of cellular damage and exhaustion.

A experimental study in Scientific Reports shows that the SARS-CoV-2 spike protein alone can trigger an autoimmune response against the ACE2 receptor - the very receptor the virus uses to enter cells.
The mechanism mirrors tissue damage seen in severe COVID-19🧵 This study is a proof-of-concept.
When the immune system reacts to the SARS-CoV-2 spike protein, part of that response can flip into autoimmunity against ACE2, the receptor the virus normally uses to enter cells.

A massive Swedish study on Nature Communications Medicine tracked 810,851 people after COVID.
Only 1.4% received an official post-COVID-19 condition (PCC) diagnosis - but that reflects only those who made it into the system.
Real prevalence of long COVID is many times higher🧵 Who was most likely to be diagnosed with PCC?
severe acute infection
unvaccinated status
female sex, older age
higher education, essential jobs (healthcare, teachers, drivers…)
pre-existing conditions - asthma, thrombosis, fibromyalgia, depression, anxiety, stress disorders

While COVID-19 (Omicron) in children is often called mild, new evidence shows a darker side.
For a small fraction who develop brain inflammation, it becomes a deadly and disabling lottery.
The Lottery of Consequences🧵 A new multicenter study in Pediatric Neurology followed 102 children with COVID-19 related encephalopathy or encephalitis.
The outcome?
Half of them either died or were left severely disabled.