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
4/ In addition, acquisition of SARS-CoV-2, or persistence of the #virus, may downregulate the #immune response so that previously dormant infections (e.g. EBV) are further “kicked up” in a manner that drives new symptoms
5/ If someone fails to clear #SARS-CoV-2 and/or immune dysfunction somehow persists after viral clearance, they may also be more susceptible to new infections. These new infections may “add into” their case - further perpetuating disease
6/ The same patterns are true of the collective organisms that inhabit our bodies. Humans harbor trillions of interacting organisms (the #microbiome) in a wide range of body sites
7/ In healthy people these microbiome ecosystems persist in a state of balance, but their activity can become dysregulated under conditions of immunosuppression or imbalance (this is called #dysbiosis)
8/ If a patient already harbors a dysbiotic microbiome at the time of SARS-CoV-2 #infection they may be less likely to clear the virus from certain body sites. For example an imbalanced #gut microbiome might predispose to SARS-CoV-2 persistence in gut tissue
9/ That is consistent with the fact that - for example - women with a more dysbiotic, imbalanced vaginal microbiome are more likely to acquire HIV: ncbi.nlm.nih.gov/pmc/articles/P…
10/ Conversely however, SARS-CoV-2 persistence in a body site like the gut, #oral cavity, #lung etc cld drive immune dysfunction in a manner that facilitates new-onset microbiome dysbiosis in that area, potentially driving new symptoms
11/ Overall then, a particular patient’s failure to clear the SARS-CoV-2 virus is very likely connected to the other persistent pathogens they harbor and to the unique activity of their microbiome ecosystems
12/ These factors differ in each patient, which could be part of why #LongCovid patients experience such a wide range of symptoms despite suffering from potential common underlying #disease mechanisms
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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
In this new paper @DrMaureenHanson argues that persistent enterovirus infection in tissue (enterovirus reservoir) may play a central role in the #ME/CFS disease process. I agree. journals.plos.org/plospathogens/…
2/ Multiple historic ME/CFS outbreaks could be explained by an enterovirus onset (outbreaks often coincided w/ outbreaks of polio), and enterovirus RNA or protein has been found in ME/CFS brain, muscle, or intestinal tissue: me-pedia.org/wiki/List_of_e…
3/ The enteroviruses are single-stranded RNA #viruses acquired via respiratory or GI infection. Infected patients can present with symptoms or experience mild/asymptomatic cases. In some patients enteroviruses infect the nervous system.
This autopsy study found #SARS-CoV-2 RNA in #vagus nerve samples obtained from severe #COVID-19 patients. Direct infection of the vagus nerve was accompanied by inflammatory cell infiltration derived primarily from monocytes: .pubmed.ncbi.nlm.nih.gov/37452829/#:~:t…
2/ Because the vagus nerve is an essential component of the #autonomic nervous system and regulates body functions such as heart rate, digestion, and respiratory rate, direct infection of the nerve by SARS-CoV-2 may contribute to related symptoms
3/ The findings beg the question 👉 Could persistent SARS-CoV-2 infection of the vagus nerve contribute to dysautonomia in #LongCovid?