Marc Veldhoen Profile picture
Mar 22 14 tweets 4 min read
Long COVID Comes Into the Light

We’re finally starting to see the truth about the vexing condition. It’s not what we thought.

#LongCovid

slate.com/technology/202…
Even before 2020’s first horrific wave of C19 deaths subsided, reports surfaced warning of a brutal second punch: Instead of recovering quickly after a mild infection, some people were suffering from symptoms that lingered or even intensified in the following weeks and months.
The first reports of how COVID seemed to fundamentally change people were scrabbled together from anecdotal accounts and preliminary studies. The picture they painted was frightening: As many as a third of all people who’d tested positive went on to report long COVID.
Few of these people had recovered much, and many were debilitated, unable to work or attend school. Newspapers and magazines ran articles that vividly described the complex litany of suffering endured by patients who weren’t getting any answers from their doctors.
Now, three years later, the research is catching up to the anecdotal reports and the early evidence, and a clearer picture of long COVID has emerged. It turns out that, like COVID-19 itself, a lot of our early guesses about it turned out to be considerably wide of the mark.
Long COVID is neither as common nor as severe as initially feared.

First reports were based on survey-based research, which has confounding factors.
a risk of selection bias; people who feel that they have LC are more likely to want to complete a questionnaire on the topic. Another is that people may report having symptoms post-COVID that they also had pre-COVID, and so their maladies may not actually have been caused by C19.
Retrospective cohort studies are better suited. Comparing two groups from electronic data, filtering out pre-COVID-19 symptoms, matching cohorts by age and sex.

bmj.com/content/380/bm…
Several of this type of studies, that take time, they are retrospective, are coming out, painting a different picture with a much more reduced incidence and severity of COVID-19 long term effects.
thelancet.com/journals/lanps…
Importantly, studies are comparing infection with SARS-CoV-2 with another infection, such as Influenza, to assess what effects may be SARS-COV-2 specific. Here finding symptoms comparable with influenza.

onlinelibrary.wiley.com/doi/10.1002/mp…
The impact on the workforce was estimated to be very considerable in the early COVID-19 days, but this has also not materialised.

theatlantic.com/health/archive…
The best available figures, then, suggest two things: first, that a significant number of patients do experience significant and potentially burdensome symptoms for several months after a SARS-CoV-2 infection, most of which resolve in less than a year;
and second, that a very small percentage experience symptoms that last longer.

i.e. LC is real, dramatically affected many people’s lives, we need to find solutions and take it very serious. But, fortunately, it has not reached the initial feared numbers.
If research funding unleashed by fears of LC ultimately explains why, then that itself would be a significant achievement—an acceleration toward the day when not only LC patients but a lot of other suffering people as well will be able to put their illnesses behind them for good.

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More from @Marc_Veld

Mar 22
Deze is wel bijzonder! Een wetenschapsontkenner, @WappieSebastian, maakt een tweet collage en zal het wel beschouwen als selluf ondersoek doen.

Het is voornamelijk gebaseerd op onbegrip van terminologie en de data. Een korte draad.
Deze komen vaal samen. Gepost door mensen die het verschil tussen beschermen (het vermindert de kans op) en stoppen (volledige preventie) niet snappen. Een helm beschermt tegen schade, maar stopt het niet. Een vaccine beschermt tegen infecties, maar kan het niet stoppen.
Ja, vaccinatie beschermt heel erg lang! Geheugen cellen worden aangemaakt, die je vele 10-tallen jaren, zo niet voor je leven bij je draagt en die je zullen beschermen tegen ernstige ziekte.

science.org/doi/10.1126/sc…
Read 11 tweets
Mar 21
Just getting this one out for some clarification.

Immune signatures underlying post-acute COVID-19 lung sequelae

science.org/doi/10.1126/sc…
"Aged hosts develop chronic lung inflammatory and fibrotic sequelae after viral pneumonia .... We hypothesized that aged individuals who survived moderate to severe acute C19 infection may experience persistent lung inflammation and fibrosis and impaired lung function."
When you are older, your immune system is weaker, responds slower, will not clear the virus as quickly, can result in higher viral titers, less control of the virus (dissemination to deeper into the lungs and other tissues), and you do not repair damage as well.
Read 11 tweets
Mar 21
What to take from the SAGO meeting?
There is new data from analysis of environmental sequencing data at Wuhan food market.
The meeting was a closed meeting as far as I understand.

The discussion is not so much, but is a step forward.
New data needs to be taken into consideration, independent on your preconceived ideas. Data, if accurate, is data, not politics.

This is the state where we are;
The new findings highlight the near certainty that (live) racoon docs and civets were sold at the Huanan Seafood Market immediately prior to the outbreak. This makes a zoonosis more likely. It is in line with previous photographic data, but pinpoints timing better.
Read 6 tweets
Mar 20
Alarming situation of emerging H5 and H7 avian influenza and effective control strategies

Review of the global avian influenza H5 and H7 status.

tandfonline.com/doi/full/10.10…
Viruses bearing the hemagglutinin (HA) gene of the H5 and H7 subtype have caused 2634 human cases around the world, including more than 1000 deaths.
These viruses have caused numerous disease outbreaks in wild birds and domestic poultry, and are responsible for the loss of at least 422 million domestic birds since 2005.
Read 6 tweets
Mar 20
Robust T cell responses to Pfizer/BioNTech vaccine compared to infection and evidence of attenuated peripheral CD8+ T cell responses due to COVID-19

Sounds ominous, but is it? Good vaccine responses but less viral responses..... or is context needed?

cell.com/immunity/fullt…
The authors characterised CD8+ and CD4+ T cell responses using SARS-CoV-2 pMHC-spheromers. These are tools to look at responses very specifically, epitopes (8-15 amino acids) from SARS-CoV-2 that are recognised by specific T cells. They used 49 epitopes, looked up to 3-4 months.
Importantly, these epitopes span the entire spike protein of 1273 amino acids. 14 are for CD8 T cells, 5 for CD4 T cells.
Then they also used 30 epitopes from 3 other genes, i.e. not Spike. They checked 351 blood samples.

This is a very comprehensive analysis.
Read 24 tweets
Mar 19
A critical analysis of the evidence for the SARS-CoV-2 origin hypotheses

The origin of SARS-CoV-2 has been the topic of substantial debate primarily because we do not have access to some relevant data. At least two major hypotheses have been suggested:

journals.asm.org/doi/10.1128/ms…
1) a natural origin through zoonosis followed by sustained human-to-human spread or
2) the introduction of a natural virus into humans from a laboratory source.

Scientific evidence alone is likely to be insufficient to provide a definitive answer.
For 2) to be substantiated would require evidence that the Wuhan Institute of Virology (WIV) was working on a very closely related CoV to the original Wuhan strain and such evidence would have to come from laboratory records.
Read 24 tweets

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