That SARS-CoV-2 is now confirmed to infect megakaryocytes long-term (studied in Long Covid patients) should definitely alarm the public health authorities everywhere.
Intent is not to doom tweet here. But we should tackle this like we did for HIV.
One thing unclear to me is whether inadvertent intravascular injection of the mRNA vaccine may change the dynamic here, allowing a larger load of MKs and then platelets to express spike — and whether that could bring about a longer term set of reactions that may mimic LC symptoms.
@CarlFle47251645 @SciDemocrat @brucep13 At any rate, for this and other reasons, I personally strongly prefer Novavax platform.
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As I’ve said for 2-3 years now, the evidence now presented by the French group:
As I’ve said all along (and to the primary investigator of this poster Dr. Bomsel personally on a call last year), someone needs to look at MKs in Long Covid;
MKs are likely the reservoir, that then pass the spike to circulating platelets in LC and cause all the consequences we see.
Conviction matters in life. I kept repeating this over and over for 3-4 years now. Got ridiculed. Called names. Told I’m a “fake doctor” and charlatan. Particularly on the serotonin’s pivotal role in acute and long COVID. We produced RCT results. We produced bench results (and more coming). I kept telling every researcher I could find about my hypothesis. And it paid off.
Clinical deterioration in COVID-19 typically occurs during the second week of illness, marked by a severe immune reaction and excessive production of pro-inflammatory cytokines such as IL-6, IL-8, TNF-α, and IL-1β. (2)
Elevations in these serum cytokines are not only predictive of and signify acute disease progression and mortality, but are also associated with a higher risk of developing post-acute sequelae of COVID-19 (PASC) #longcovid. (1, 2, 7)
Repurposed drugs with host-directed antiviral and immunomodulatory properties have shown some promise in the treatment of COVID-19, but most trials have used monotherapy with a single agent.
Few trials have studied combinations of these agents.
... the production of pathogenic afucosylated antibodies against the spike protein.
First, some introduction in order to better understand the premise and the findings of this work:
In the last 3 years, an exhaustive amount of research has been carried out to elucidate the precise events that directly cause progression of COVID from an early mild acute illness in the first few days, to a severe/fatal form in a subset.
SARS-CoV-2 most definitely infects the bone marrow.
Not only in the acute infection.
But also chronically, the spike protein is found present in the bone marrow on autopsies of patients who died for other reasons.
I wish I could share more, but ...
... we are actively investigating and have some very intriguing findings on how the infection of the bone marrow by SARS-CoV-2 brings about the gear shift from early mild disease -> to severe COVID.
This ties the various parts of disease pathophysiology in a convincing manner.
It is absolutely *necessary* for various research groups focusing on #longcovid to study the bone marrow in those afflicted by severe LC to assess which cell lines harbor SARS-CoV-2 or its protein remnants.