Zdenek Vrozina Profile picture
Apr 7 • 12 tweets • 2 min read • Read on X
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 levelđź§µ
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.
That matters because these symptoms are not trivial.
In the study, phantosmia and parosmia were the strongest independent predictors of reduced quality of life. Around 41% of those with smell and taste disorders also reported decreased life satisfaction.
And for many people, these problems did not simply fade away.
Depending on the symptom, roughly half or more reported that things had stayed the same or even worsened since onset.
This is where the discussion gets more important.
Smell is not just the nose. Smell signals travel through neural pathways into brain regions involved in perception, memory, and emotion.
So when smell remains disturbed long after infection, that points to ongoing dysfunction in a neuro-sensory system, not just an annoying leftover symptom.
Yes, this study does not by itself prove structural brain damage.
But it fits very well into the broader picture, because longitudinal MRI studies after COVID have already described changes in regions linked to smell processing - including the orbitofrontal cortex and the parahippocampal gyrus.
So persistent smell and taste disorders after COVID are consistent with ongoing dysfunction of the olfactory pathways and fit with studies that have already described brain changes after COVID.
Smell is probably only the part we can see more clearly. People notice it quickly, it is relatively easy to measure, and it is harder to dismiss than many other lingering effects.
In other words. Smell dysfunction is the visible tip of a much bigger post-COVID burden.
Rehman at al., Self-Reported Smell and Taste Disorders in the General Population: A Cross-Sectional Survey in Austria, Germany and Switzerland. researchgate.net/publication/40…

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More from @ZdenekVrozina

Apr 7
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 exceptionalđź§µ
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).
Read 13 tweets
Apr 6
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 - apoptosisđź§µ
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.
Read 9 tweets
Apr 4
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 pathwaysđź§µ
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.
Read 13 tweets
Apr 3
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.đź§µ
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!
Read 14 tweets
Apr 2
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 othersđź§µ
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.
Read 25 tweets
Apr 2
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 dysfunctionđź§µ
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.
Read 13 tweets

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