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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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.
The Karaviti study is finally in print, which makes this a good time to revisit it. It shows that subclinical myocardial injury in children after COVID-19 may not be something exceptional🧵
The key point is often missed. This was not mainly a comparison of children with Long Covid versus children without Long Covid. It compared
children after COVID-19
healthy controls without prior SARS-CoV-2 exposure
In that comparison, conventional echocardiographic measures did not differ significantly, but the post-COVID group showed worse left ventricular global longitudinal strain (LV GLS).
A new paper looks at shared molecular mechanisms between COVID-19 and Parkinson’s disease. It does not show that COVID causes Parkinson’s.
What it does ask is whether the two conditions share biologically meaningful pathways🧵
The authors identified 77 overlapping differentially expressed genes across COVID-19 and Parkinson’s datasets. The main signal points to inflammation-related pathways plus signs of dopaminergic neuron dysfunction!
Their main candidate is CHI3L1. In the single-cell analysis, CHI3L1 was especially elevated in astrocytes from severe COVID-19 brain tissue, which led the authors to propose an astrocyte - CHI3L1 - neuroinflammation axis as one possible explanation for why infection might worsen neurological outcomes.
A new population based study from Stockholm sends a pretty troubling signal.
During follow-up, a cardiovascular event occurred in 20.6% of men and 18.2% of women with diagnosed long COVID.🧵
In the control group without long COVID, the numbers were much lower. 11.1% for men and 8.4% for women.
These were not mainly patients recovering from severe acute COVID or ICU stays. The study focused on non-hospitalized adults aged 18-65 with no prior cardiovascular disease!
A new 2026 paper looks at a possible mechanism behind rare myocarditis after COVID-19 mRNA vaccination.
Not vaccines broadly damage the heart.
More like
some people may be biologically more vulnerable than others🧵
The paper’s central idea is mitochondrial vulnerability.
In simple English
your mitochondria can seem mostly fine under normal conditions, but still handle stress badly when the system gets pushed.
That matters because this study is trying to explain a rare adverse event, not argue that this is happening across the whole population.
That distinction is everything.
This new important preprint study makes a strong mechanistic case that the SARS-CoV-2 E protein localizes to mitochondria and is linked to concrete mitochondrial dysfunction🧵
It pushes E beyond the idea of being just a structural protein involved in viral assembly. The paper suggests it may also directly disrupt host-cell function at the mitochondrial level.
The authors connect several findings into one coherent picture. Mitochondrial localization of E, reduced membrane potential, impaired respiration, increased ROS, and broad lipid/metabolic changes.