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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