People are asking me: what if we did a similar autopsy study to look for #viruses in ME/CFS? Well, several teams that performed single autopsy studies on #ME/CFS patients found evidence of persistent enterovirus infection in subject brain/body tissue
2/ Enteroviruses are (like SARS-CoV-2) single-stranded RNA viruses. They include the coxsackieviruses, poliovirus, echoviruses + rhinoviruses. These viruses cause about 10–15 million #infections each year in the USA alone
3/ This 1994 ME/CFS autopsy study identified positive PCR sequences with similarity to coxsackievirus B3 in samples from the #brainstem and hypothalamus (and also in muscle and heart tissue): acpjournals.org/doi/10.7326/00…
4/ This 2001 ME/CFS autopsy study found enterovirus VP1 protein in small blood vessel fibroblasts of the cerebral cortex + a patchy distribution of the VP1 protein in a small fraction of brain glial cells: tandfonline.com/doi/abs/10.130…
5/ In 2015 Dr. John Chia presented an ME/CFS autopsy report at a scientific conference where he found #enterovirus RNA in the brainstem, lateral frontal cortex, occipital lobe + cerebellum. However results were never formally published.
6/ It blows my mind that the ME/CFS research community has largely not followed-up on these findings. There has been little interest in autopsy studies generally, let alone studies that look for #virus in the brains/bodies of patients
7/ At @polybioRF we are working to change that. We are trying to set up an innovative postmortem (autopsy) #ME/CFS research program. If you are a scientist who wants to get involved, or a private donor who wants to support the effort let us know!
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New preprint: The team did autopsies on 44 patients w/ #COVID-19 to map + quantify SARS-CoV-2 distribution, replication and cell-type specificity across the human body (including brain) from acute infection through over 7 months following symptom onset: researchsquare.com/article/rs-113…
2/ They found that #SARS-CoV-2 was widely distributed, even among patients who died with asymptomatic to mild COVID-19. They also detected persistent SARS-CoV-2 RNA in multiple anatomic sites, including regions throughout the #brain, for up to 230 days following symptom onset
3/ Persistence of low-level #SARS-CoV-2 RNA was frequently detected across multiple #tissue categories among all late cases patients who passed away after 31 days, despite being undetectable in plasma
New @polybioRF podcast! I interviewed Dr. Resia Pretorius: Department Head/Research Professor at Stellenbosch University in South Africa. Listen on an App like Spotify () or watch on Youtube ()
2/ In the interview Resia talks about how her research team has identified microclots resistant to fibrinolysis + hyperactivated platelets in the blood of #LongCovid patients. We also discuss how we are planning to extend the research to #ME/CFS
3/ When it comes to the LongCovid microclots, Resia describes her earlier research showing that platelets (blood cells that contribute to #clotting) have receptors that recognize a wide range of viral, bacterial, and fungal proteins or products
I want to put this study on everyone's radar b/c I think it's a genuinely cool opportunity for people/patients to get high-quality data on their #SARS-C0V-2 #immune status over time👇 (I have no financial ties to the company).
2/ To be more clear about what the study involves, the @serimmune team will assess each subjects’ individual immune response to SARS-CoV-2 from both natural #infection and #vaccination for up to 5 years.
3/ If you register for the study, Serimmune will send you a sample collection kit that allows you to collect your blood at home. Then you simply mail the sample to their lab using the pre-paid envelope provided.
For this new @polybioRF podcast I interviewed Dr. Liisa Selin, professor of pathology at the University of Massachusetts Medical School. Listen on an App like Spotify (open.spotify.com/episode/5rdB0G…) or watch on youtube ()
2/ Liisa talks about her work as a #viral immunologist, and how her team recently got an NIH grant to study the role of viral infection and T-cell exhaustion in #ME/CFS. She discusses existing data on the topic and how the research may also inform the #LongCovid disease process
3/ Liisa and team are fundraising to further extend their research to LongCovid. Donate here to support her efforts: classy.org/fundraiser/321…
In our recent review on #LongCovid/PASC we bring up the possibility that dysbiosis or imbalance of host #microbiome communities (in ecosytems such as the gut, lungs, or oral cavity) might contribute to at least some LongCovid symptoms: frontiersin.org/articles/10.33…
2/ More specifically immune dysregulation driven by #SARS-CoV-2 might allow pathobionts (bacteria capable of both commensal + virulent acitivty) in the gut, mouth, or other body sites to collectively shift towards a state of imbalance + pro-inflammatory gene/metabolite expression
3/ Conversely, b/c composition + activity of the microbiome can influence host susceptibility and ongoing control of #viral pathogens, exisiting microbiome dysbiosis in a range of body sites may serve as a form of predisposition to LongCovid
Sometimes I hear people dismiss the possible role of a persistent #pathogen (such as a herpesvirus) in the development of a chronic #disease b/c the same pathogen can be found in healthy people
2/ I see it differently 👉 While the presence/absence of a persistent pathogen in a patient with chronic symptoms matters, the real question is: what is the pathogen doing? Is its ACTIVITY different in patients vs. healthy people?
3/ More specifically, in the #patient with chronic symptoms is the pathogen expressing different #proteins/metabolites? And are these proteins/metabolites increasingly interfering with human gene expression, metabolism, and the immune response?