Another study where long COVID does not look like a small residual problem after infection, but like broad chronic illness scattered across everyday medicine.
And that is exactly why the system often fails to see it🧵
The study analyzed data from 58 US hospitals.
The algorithm identified PASC in 16.28% of patients after COVID.
Roughly 1 in 6!
The most important part is not only how many people have long COVID.
It is that most of the detected manifestations were not short acute episodes.
They were mostly chronic or potentially chronic conditions.
The more important number is this -
14.54% of all post-COVID patients had chronic PASC burden!
That is not a few weeks of cough after a virus.
That means long-term care, follow-ups, specialists, tests, medication, and work limitations.
The cumulative prevalence of PASC did not decline.
It slightly increased through mid-2024.
The authors interpret this as an accumulating burden, not just the fading tail of early pandemic waves.
Long COVID often does not appear in the system as long COVID.
Instead, the patient shows up
to primary care with fatigue,
to cardiology with dysautonomia or palpitations,
to endocrinology with a new metabolic problem,
to neurology with cognitive symptoms.
And this is the coding problem.
Many of these patients are not coded as long COVID/PASC. They are coded under the specific diagnosis they present with. Fatigue, palpitations, dysautonomia, cognitive symptoms, respiratory problems, abnormal glucose, prediabetes, or other chronic conditions.
Without a connecting code, the burden fragments into many ordinary diagnoses.
The system then fails to see it as post-infectious chronic disease, even while it is already carrying it clinically.
That is the real strength of this study.
It challenges the illusion we don’t see long COVID, so it isn’t there.
The opposite is true.
Part of the burden is already inside the system, just split across diagnoses and specialties.
Healthcare does not need to report a collapse of long COVID clinics to be under pressure.
The burden can show up as more prediabetes/diabetes, more fatigue syndromes, more neurology visits, more cardiology complaints, and more respiratory problems.
The system is treating it.
It just often cannot see the common denominator.
Long COVID does not have to overwhelm healthcare under one label.
It can burden it as thousands of ordinary diagnoses without a shared code.
There was no COVID-negative control group, and some variation may reflect coding practices.
But the signal is large.
After COVID, we are seeing broad, long-term, poorly coded illness.
And if we cannot name it properly, that does not mean it does not exist.
It means we are measuring it badly.
And it may also mean we are treating it poorly.
If post-COVID illness is fragmented across specialties without a shared framework, patients may receive treatment for isolated symptoms while the underlying post-infectious process remains unrecognized. @szupraha @ZdravkoOnline @adamvojtech86
Fragmented recognition often leads to fragmented care.
This new study does not matter because IgG transfer is a new concept.
But because it pulls several pieces into one mechanistic chain - Long COVID patient IgG, tissue autoreactivity, Fc-mediated immune function, small fiber damage, pain/fatigue-like pathology, and CNS activation🧵
The authors used several independent methods. Tssue staining, proteome arrays, ELISA, IgG pull-down, mass spectrometry.
They found a broad range of autoantibodies in people with Long COVID.
A striking part of the signal pointed toward the nervous system.
Patient IgG reacted with tissues such as the locus coeruleus, thalamus, meninges, sciatic nerve, and also peripheral tissues including the thyroid, adrenal gland, heart muscle.
That matters because so many Long COVID symptoms are neurological, autonomic, or endocrine.
This paper is interesting because it identifies a concrete neurochemical signal in the CNS that connects long COVID/PASC, PEM, fatigue, and reduced physical endurance - lower activity of the central noradrenergic pathway in cerebrospinal fluid🧵
The study asked whether post-infectious ME/CFS and long COVID/PASC show measurable abnormalities in central catecholamine systems - specifically the norepinephrine and dopamine pathways.
The authors looked directly at neurochemical markers.
Not just another symptom description paper.
They measured catecholamines and their metabolites in cerebrospinal fluid.
For the norepinephrine pathway
norepinephrine + DHPG + MHPG
For the dopamine pathway
dopamine + DOPAC + HVA
So the point was not to rely on one isolated molecule, but estimate broader pathway activity.
This new paper may be the most direct evidence so far that the SARS2 protein ORF3a can travel from the lungs to a distant organ through exosomes - in this case, the liver.
This is not a small detail. It may be one mechanism behind systemic COVID🧵
The point is not simply
Is the virus in this organ, yes or no?
The point is more uncomfortable
SARS2 may remain mostly in the respiratory tract, while some of its proteins travel elsewhere - and still affect distant organs.
The paper studied 133 patients with mild SARS2 infection and 63 negative controls in Shanghai, February 2024.
More than half of the COVID-positive patients had abnormal liver tests, mainly AST, ALT, and GGT.
This may be one of the more important long COVID papers in a while.
A new study in Frontiers in Immunology suggests that COVID can trigger new-onset insulin resistance - and that this may drive abnormal NETosis in neutrophils months after infection🧵
NETosis is the process where neutrophils release web like structures made of DNA, histones, enzymes.
Normally, this helps trap pathogens.
But when excessive, NETs can -
damage the endothelium
trigger microclots!
amplify inflammation
activate coagulation.
Exactly the kind of pathology seen in COVID.
The study followed 60 COVID patients.
Among 36 people without prior glucose metabolism problems, 24 developed insulin resistance 4 months after infection.
That alone is a striking finding.
Important new study. ME/CFS and Long COVID are not the same thing.
Yes, they can look very similar from the outside - crushing fatigue, PEM, brain fog, dysautonomia.
But when researchers looked deeper into the immune system, the biology looked different🧵
The study compared
103 people with ME/CFS
63 people with Long COVID
41 healthy controls
They used detailed immune profiling of blood cells - especially monocytes, dendritic cells, and T-cell subsets.
Long COVID
The immune system looked chronically activated, but also exhausted.
Almost like a system that has stayed switched on for too long and is no longer working efficiently.
Some children with Long COVID seem to fall into the same trap as adults - and medicine still doesn’t really know how to get them out.🧵
The UK CLoCk study followed young people who had already been living with post-COVID symptoms for two years. Another 1.5 years later, most of those who responded still met the definition of post-COVID condition.
Some describe years of exhaustion, brain fog, sleep problems, breathlessness, pain, and symptoms that come and go without warning.
No slow recovery after a virus.