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.
Pretorius also argues these aggregates could do more than just flag biology.
They may help stratify disease severity and monitor response to treatment - which is a big deal if Long COVID is going to move toward more measurable, blood-based assessment.
This signal is not just an age effect.
In the healthy group, these aggregates rose somewhat with age. In the Long COVID group, the baseline was already elevated, regardless of age.
The idea that Long COVID may be measurable in blood no longer sounds far-fetched.
Thompon at al., An imaging flow cytometry method to study platelet-monocyte aggregates using Long COVID as a model. biorxiv.org/content/10.648…
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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.
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).
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.
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.