This study suggests a possible mechanism for how SARS-CoV-2 could harm neurons in the inner ear.
Not mainly through inflammation, but potentially through a more direct effect on spiral ganglion neurons, involving disrupted mTOR signaling, abnormal stress granules, and eventually - apoptosis🧵
That matters because spiral ganglion neurons are not some minor supporting cells. They are the neurons - that carry sound information from the cochlea into the auditory pathway.
If they are damaged, the problem is not just in the ear. It affects the neural transmission of sound itself.
The authors try to map out an actual chain of events. In their model, infection - and especially spike related effects - seems to disturb the cell’s stress-response machinery.
Stress granules start accumulating abnormally, mTOR signaling drops, and the neuron is pushed closer to cell death.
And that pushes back against the overly simple idea that all post COVID damage must be just inflammation. This paper argues that at least some injury may happen inside the affected nerve cells themselves.
Anti-inflammatory treatment alone may not always be enough.
This is not a final clinical proof in humans. It is mainly a mechanistic study in transgenic mice and cell culture.
Still, it raises an important question. If SARS2 or spike driven cellular stress - can damage ganglion neurons in the inner ear, then it is reasonable to ask whether other vulnerable neural structures might also be affected in similar ways!
So it does support a broader hypothesis worth taking seriously - that mechanisms like disrupted stress responses, impaired mTOR signaling, and apoptosis may not be limited to one tiny corner of the nervous system.
We need better answers - if SARS2 can plausibly injure inner-ear neurons directly, then the bigger question is whether similar mechanisms may be affecting other parts of the nervous system too, including the brain.
Liu at al., SARS-CoV-2 directly infects the inner ear and causes hearing dysfunction. cell.com/cell-reports/f…
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COVID-19 is not just a story of inflammation. This review argues that it is also a story about what SARS2 does to mitochondria - and how that can turn infection into energy failure, cell injury, and worse oxygenation. This is an important mechanistic review🧵
Mitochondria are not framed here as passive bystanders damaged late in severe illness. In this model, they are active participants in disease - they shape ATP production, ROS, apoptosis, and oxygen sensing.
The review describes two main routes of damage -
very early changes in expression of mito-related genes (hours)
direct interactions between viral proteins and host mito proteins.
So not just the cell is stressed, but a more specific viral rewiring of core cell machinery.
This interesting paper lays out a very specific idea for how severe COVID-19 may be driven not only by the virus itself, but by the way the immune system handles what the virus leaves behind🧵
The starting point is simple.
SARS2 can leave behind viral RNA and nucleocapsid protein (N). N naturally binds viral RNA, and during infection people also make antibodies against N.
The authors build the story from there.
Viral RNA + nucleocapsid (N) + anti-N IgG
= an immune complex carrying viral genetic material.
Can Long COVID show up in a blood sample?
A new preprint @resiapretorius suggests it might. Researchers found much higher platelet-monocyte aggregates in people with Long COVID than in healthy controls - about 29% vs 4.6%🧵
That is a striking signal, and it hints that Long COVID may leave a measurable trace in blood.
In healthy controls, a monocyte was more likely to have just one platelet attached. In Long COVID, researchers more often saw multiple platelets attached to a single monocyte.
Why does that matter?
Because platelet-monocyte aggregates sit right at the intersection of clotting and inflammation. When they rise, it can point to ongoing thromboinflammatory activity - in simple words, blood clotting biology and immune signaling feeding into each other.
Long COVID research badly needs studies that move beyond description and toward intervention. This is why this preprint is worth attention. It starts to sketch a possible treatment path.🧵
A new preprint is interesting because it points to something important
a potentially treatable biological mechanism.
Not a clinical breakthrough. More like a promising preclinical proof of concept.
This study is a strong mechanistic signal that at least some of the neurological problems after COVID may be driven by persistent neuroinflammation - and that shifting immune regulation can improve that state in mice.
Do you have hypertension?
This study in Nature suggests that for people who already had hypertension before getting COVID, the infection was linked to a higher long-term risk of serious cardiovascular events.🧵
In people with hypertension, an infection can leave behind - or speed up - processes that raise the risk of cardiovascular disease over the months and years that follow.
The excess risk was more pronounced in people with poorer blood pressure control at baseline, and that signs of a stronger acute inflammatory response during infection predicted worse long-term outcomes.
Another piece of the puzzle. Post-COVID changes are not just an isolated problem affecting a few unlucky individuals. They appear to have consequences at the population level🧵
A striking headline from Austria - 4 in 10 people report smell or taste problems.
That figure comes from a new cross-sectional survey of 2340 adults in Austria, Germany, and Switzerland looking at self-reported smell and taste disorders after the COVID era.
The key point is that this was not mainly about complete smell loss.
The most commonly reported problems were olfactory intolerance, phantosmia, and parosmia - in other words, abnormal, distorted, or intrusive smell experiences.