Very interesting! 👉 Team found (in mice) that #fever alters surface proteins (integrins) on #immune cells such as lymphocytes + macrophages ☝️ These changes allow such cells to better travel via #blood vessels to reach sites of infection.
And yet, if you walk into a USA #pharmacy, most medications for flu, colds, inflammation, injuries etc deliberately “knock down” #fever to temporarily palliate symptoms 👉 How do such #medications then impact long-term immunity, pathogen persistence and #microbiome health??
This same trend (medications that treat the #immune response as an “enemy” vs. an “ally”) are also “standard of care” for chronic disease 👉 But as such “#autoimmune”/inflammatory conditions are increasingly tied to #microbiome dysbiosis does that paradigm still make sense??
In this paper I argue that the answer is NO 👉 Immunosuppression is a failed #treatment paradigm for chronic inflammatory #disease 👉 In fact, our over-use of immunosupressive drugs is driving issues like #antibiotic resistance and co-morbid conditions: discoverymedicine.com/Amy-D-Proal/20…
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Tell @ChrisCuomo that 33 scientists from 14 institutions joined forces to write this paper documenting evidence for #SARS-CoV-2 persistence as a potential driver of #LongCOVID. We call for more clinical trials of drugs capable of clearing persistent virus: pubmed.ncbi.nlm.nih.gov/37667052/
2/ We have formed a global #Consortium to study SARS-CoV-2 persistence: to determine if reservoirs of the #virus in LongCOVID tissue can drive widespread dysfunction including clotting, #microbiome, and neuroimmune abnormalities: polybio.org/longcovid
3/ Thus far, members our Consortium or our colleagues (including at NIH) have found persistent #SARS-CoV-2 RNA or proteins in tissue/nerve samples collected from dozens of human body & brain locations: pubmed.ncbi.nlm.nih.gov/36517603/
I want to add that I see #SARS-CoV-2 persistence as part of a larger picture in which other latent pathogens and/or #microbiome organisms also harbored by a patient play an important role in the ultimate set up symptoms they develop
2/ Pathogens harbored by a patient at the time of SARS-CoV-2 #infection may serve as a predisposing factor to either persistence of the virus or increased disease in the acute phase
3/ E.g. Bartonella is a persistent #bacteria that drives blood vessel dysfunction by infecting #vascular endothelial cells. So someone with Bartonella may be more susceptible to SARS-CoV-2’s detrimental impact on blood vessels, and have more trouble clearing virus from such sites
Incredible to see the technology being developed openly here - not just to mitigate #COVID-19 but to create an innovative global infrastructure that positions humanity in excellent shape to combat the next airborne #virus pandemic
2/ To advance this movement in which novel tools to study & contain airborne #pathogens are actively being built, one must reject the narrative that there are only two paths forward 1) To 'care' abt airborne #infection means lockdowns 2) Freedom means ignoring airborne infection
3/ It's 2023 and many intermediate solutions are possible. We can install UV light and filter #technologies in schools, airports, even homes - to remove viruses from the air. With enough of these tools in a room, people may be able to interact freely without getting infected
Incredible new paper demonstrating #SARS-CoV-2 persistence + associated immune modulation in macaque monkeys. The team found replication competent SARS-CoV-2 virus in macaque lung alveolar #macrophages beyond 6 months postinfection: nature.com/articles/s4159…
2/ IFN-γ production was impaired in NK cells from macaques with persisting virus. Moreover, IFN-γ also enhanced the expression of major histocompatibility complex (MHC)-E on lung alveolar macrophages, possibly inhibiting NK cell-mediated killing
3/ In the lab, increasing SARS-CoV-2 levels during culture corresponded to ongoing viral replication and were accompanied by #virus-induced morphological changes including filiform extensions that connected multiple macrophages, with viral proteins detected in these extensions.
This new preprint found that exposure + antibody responses to previous Coronaviruses may modulate the NeuroPASC (#LongCovid) immune response in a manner that could make such patients less likely to clear the SARS-CoV-2 virus: medrxiv.org/content/10.110…
2/ Specifically, they found that neuroPASC patients exhibited attenuated systemic antibody responses against #SARS-CoV-2, characterized by decreased capacity to activate antibody-dependent complement deposition, NK cell activation + to bind Fcγ receptors
3/ The neuroPASC patients also showed significantly expanded antibody responses to other common #Coronaviruses including 229E, HKU1, NL63 and OC43
I am excited to share our new position paper on #SARS-CoV-2 reservoir (viral persistence) in Long COVID or post-acute sequelae of COVID (PASC): nature.com/articles/s4159…
2/ We review evidence showing that some Long COVID patients may not fully clear the SARS-CoV-2 #virus after acute infection. Instead, replicating virus and/or viral RNA - potentially capable of being translated to produce viral proteins - persist in tissue as a "reservoir"
3/ Evidence for SARS-CoV-2 reservoir in Long COVID includes studies that have found SARS-CoV-2 RNA or protein in Long COVID tissue samples collected months after acute #COVID-19. Immune responses indicative of a SARS-CoV-2 reservoir have also been documented in #LongCovid