"Zombie" #COVID19 fragments linger for some, causing severe disease outcomes, new research reveals
A new finding could be the reason why some people have long COVID or die from SARS-CoV-2
By Nicole Karlis
Published February 2, 2024 3:02PM (EST)
"This suggested that more serious COVID-19 outcomes are a result of these leftover fragments that are essentially overstimulating the immune system."
#LongHaul #LongHaulCovid #LongCovid #HyperInflammation #CovidIsntOver
TANK-binding kinase-1 (TBK1) and its homologue IκB kinase-ε (IKKε) are critical in the induction of the interferon response and the response to infection by pathogens. Here the authors show that pharmacological targeting of TBK1 AND IKKε reduces the immunopathology seen in a murine model of SARS-COV-2 infection.
Importance of noting all clinical observations, even when not intended -> discovery of metoprolol as an IL-6 antagonist... (well, inhibition of IL-6 translation).
Therapeutic benefit in CAR-T cell-associated cytokine release syndrome (CRS).
Intriguing in vitro effect limited to stimulation by CAR-T lysate & not LPS. Hard to know if experiments really comparable, in terms of timing and stimulus
@JExpMed #immunology #hematology #Science #medicine #Hyperinflammation
This study repurposes metoprolol, a WHO-essential drug, as a potentially safe and effective medication for chimeric antigen receptor (CAR) T–induced human cytok
More evidence of #trainedimmunity in #COVID19 / #SarsCoV2 infection leading to #Hyperinflammation
#immunology #virology #infectiousdiseases #IDMastodon #medicine
Secukinumab blocks IL-17 and some evidence of efficacy in hidradenitis suppurativa in 2x RCT.
Interesting in so much this is clearly an inflammatory disease in which there is also undoubtedly an infective component.
These studies, along with efficacy of TNF blockade indicates hyperinflammation the main issue.
#immunology #inflammation #hidradenitis #IL17 #secukinumab #RCT #trial #hyperinflammation
Pretty stunning paper proposing a mechanism for #MIS-C in children post-Covid-19.
Genetic deficiency in OAS–RNase L promotes myeloid cell cytokine production +++.
#COVID19 #immunology #inflammation #hyperinflammation #science #ScienceMastodon
DoomsdaysCW
Giuseppe Michieli
Gabriele Pollara
Katja Masjosthusmann