It’s important to acknowledge that vaccinated people can acquire/transmit the Delta variant. While vaccinated individuals should experience less severe acute #COVID-19, they may still be at risk for LongCovid/PASC (which has been shown to develop after asymptomatic/mild COVID-19)
2/ For example, this team reported a range of long-term symptoms in a cohort of previously confirmed or presumed COVID-19 patients whose acute symptoms were largely managed without the need for hospitalization: medrxiv.org/content/10.110…
3/ This preprint documented persistent COVID-19 symptoms in 1,407 subjects with confirmed #SARS-CoV-2 infection. ∼32% of subjects reporting symptoms at 61+ days after infection were asymptomatic at the time of initial SARS-CoV-2 testing: pubmed.ncbi.nlm.nih.gov/33688670/
4/ Similarly, as discussed in this @nytimes article, studies have found that up to 75% of children who develop post-COVID multisystem inflammatory syndrome (#MIS-C) were asymptomatic during their initial COVID-19 illness: google.com/amp/s/www.nyti…
5/ It follows that to keep #LongCovid/PASC and #MIS-C cases to an absolute minimum, even vaccinated individuals should be wearing masks whenever possible. And since SARS-CoV-2 is spread via aerosol transmision, N95s masks should be strongly prioritized
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@MBVanElzakker and I are excited that our new paper on biological factors that may contribute to the development of LongCovid/PASC was published today: frontiersin.org/articles/10.33…
2/ The paper details mechanisms by which RNA #viruses beyond just #SARS-CoV-2 have be connected to long-term health consequences.
3/ It also reviews literature on acute #COVID-19 and other virus-initiated chronic syndromes such as post-#Ebola syndrome or #ME/CFS to discuss different scenarios for #LongCovid/#PASC symptom development.
In a meeting I watched today, microglia priming was mentioned in #LongCovid and #ME/CFS. It’s important to clarify what “microglia priming” means. Microglial priming does not mean that after a trigger has “cleared” microglia remain perpetually activated
2/ Instead, microglia priming goes like this 👉 When microglia or other glial cells detect #infection, injury, or inflammatory mediators, they enter a state of activation in which they change morphology and release their own neuroexcitatory inflammatory mediators
3/ Then, after activating, they retain a “primed” functional state which causes an even more robust response to *subsequent* infectious/immune/#inflammatory challenges. And as cells, microglia live long lives (they are not replaced as often as many other cell types)
Thanks @DrDavidACox for interviewing me for this article on #LongCovid. There’s also great info in the article on research showing #viral RNA in the brains of patients w/ post-SARS syndrome, and viral reservoirs in patients w/ post-Ebola Syndrome: bbc.com/future/article…
2/ The article reads: “Amy Proal, a microbiologist who runs the @polybioRF which studies the causes of chronic inflammatory diseases, believes that small amounts of #pathogens that linger beyond the reach of the immune system in remote pockets of the body...
3/ “...known as reservoirs or anatomical sanctuaries, are at least partially responsible for a whole range of post-infectious syndromes. This includes long #Covid, but also a number of mysterious illnesses which have puzzled scientists for decades, such as chronic Lyme disease..
Preprint reports elevated serum inflammatory cytokine profile in #LongCovid subjects. Worth noting that an ongoing immune response towards persistent viral reservoirs of #SARS-CoV-2 and/or antigen could explain the findings: medrxiv.org/content/10.110…
2/ So the findings underscore the need to do studies that obtain tissue (via surgery or biopsy if possible) to search for #SARS-CoV-2/antigen in #LongCovid patients. Similar to what this team did (and found viral RNA/antigen in multiple tissue types!): gut.bmj.com/content/early/…
3/ Studying both the LongCovid immune response AND possible #viral reservoirs is very important for LongCovid patients to get the best treatment. If you assume the #immune response alone is the problem, standard of care could become immunosuppressive drugs
If you’re considering studying blockage of GPCRs in #LongCovid or related conditions, please start w/ the understanding that humans are not sterile...and that common human organisms/pathogens express proteins/metabolites that block/dysregulate GPCR signaling
2/ Herpesvirus re-activation is common in #COVID-19, and may impact some LongCovid cases. The herpesviruses alone (EBV, CMV etc) create a wide range of proteins that block GPCR signaling: ncbi.nlm.nih.gov/pmc/articles/P… Indeed, viral hijacking of GPCRs is a big topic in cancer research
3/ Beyond that, many commensal #bacteria derived from the human #microbiome appear capable of expressing metabolites that are GPCR mimics, that directly impact GPCR signaling. That means even changing microbiome dynamics could impact GPCR-related issues: ncbi.nlm.nih.gov/pmc/articles/P…
Happy 2021! @MBVanElzakker and I are excited to share our new article published in #Immunometabolism: “Pathogens Hijack Host Cell Metabolism: Intracellular Infection as a Driver of the Warburg Effect in Cancer and Other Chronic Inflammatory Conditions”: ij.hapres.com/htmls/IJ_1341_…
2/ In the paper, we detail molecular mechanisms by which #viral, #bacterial, and #parasite intracellular pathogens can induce, or contribute to, a Warburg-like #metabolism in infected host cells in order to meet their own replication and nutritional needs.
3/ We also discuss how host defense towards #infection may impact cellular metabolic changes (including how #mitochondria can participate in the innate immune response towards infection)