This interesting study found that skeletal #muscle cells of #ME/CFS patients showed a decrease in oxidative phosphorylation (a metabolic pathway used by #mitochondria to generate #energy). In simple terms, that caused the cells to have a dysregulated #metabolism.
2/ Not mentioned in the paper, but important to consider, is that most well-studied #viral + bacterial #pathogens “hijack” the metabolism of the cells they infect in a manner that can result in decreased oxidative phosphorylation (or similar changes in cell energy pathways).
3/ In simples terms, these #pathogens “hijack” cell metabolism to “pull” substrates out of the human mitochondrial energy pathways...and use the substrates (lipids, fatty acids, amino acids) for their own #nutritional and replication purposes!
4/ To better understand that trend check out these papers: 1) This one describes key mechanisms by which #viruses like EBV/CMV hijack host cell metabolism: bmcbiol.biomedcentral.com/articles/10.11… 2) This one explains how many bacterial pathogens can do the same: febs.onlinelibrary.wiley.com/doi/full/10.11…
5/ Ultimately what that means is that in conditions like #ME/CFS increasingly tied to host cells with altered #metabolic function...we should study if the #pathogens patients can harbor may be driving some of those metabolic changes!
6/ And does the trend matter for patients w/ Chronic #Lyme Disease? You bet! This paper is just one example of how #Borrelia dramatically alters the metabolic profile of the immune cells it infects: sciencedirect.com/science/articl…

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More from @microbeminded2

11 Oct
@sickanddamned @__ice9 @GemzME @Cov19longtail @VirusesImmunity @MBVanElzakker Walker hi - I very much disagree that #Borrelia or #EBV are typically ” long gone” in infected patients who develop chronic symptoms.
@sickanddamned @__ice9 @GemzME @Cov19longtail @VirusesImmunity @MBVanElzakker 2/ There is a large body of literature showing that even if such #organisms cannot be found in blood, they can persist in certain tissues or the central #nervous system where they are very hard to identify clinically
@sickanddamned @__ice9 @GemzME @Cov19longtail @VirusesImmunity @MBVanElzakker 3/ This is particularly obvious w/ EBV which is a #herpesvirus. Herpesviruses almost never “clear” after #infection, and symptom resolution is due to the immune system’s ability to contain the #virus in a non-replicating state
Read 10 tweets
30 Sep
Boy is it refreshing to read this thread that takes a close look at two studies being used to rationalize #vitamin D supplementation for #COVID-19. It explains how both studies have so many problems that the findings must be interpreted with great caution
2/ Why do I care? I spent part of my graduate work working on the molecular #biology of the vitamin D system (including how the various “vitamin” D metabolites impact Vitamin D Receptor activity/gene expression)
3/ Far from being simplistic “vitamins”, the various forms of “vitamin” D are actually secosteroid transcriptional activators, w/ 1-25-dihydroxyvitamin D (also called D3) also acting as a hormone
Read 11 tweets
2 Sep
Thanks for sharing my perspective in this piece @MeganEDoherty! As I mention, in these #longcovid cases, it’s very important to take the potential persistence of #COVID-19 in certain tissues and/or the central nervous system (CNS) seriously!
2/ That’s b/c #Coronaviruses have been shown capable of persisting in human #tissue or certain “anotomical sanctuaries” - for example, this team found Coronavirus RNA + antigen in the Multiple Sclerosis brain: ncbi.nlm.nih.gov/pmc/articles/P…
3/ Also in other “post-viral” syndromes like “Post-#Ebola Syndrome, viral RNA has been found in unexpected body sites like sperm, or the eyes, years after initial infection: nejm.org/doi/full/10.10…
Read 6 tweets
19 Jul
Ryan I take issue with your rash conclusion that #COVID-19 cannot survive in a persistent form in certain #LongCovid patients, and it's unfair to say that people studying the topic or discussing the possibility of COVID-19 chronic persistence are spreading rumors or causing harm!
2/ First, there is no way for you to *know* that #COVID-19 cannot persist in a latent/chronic form in certain patients. The #virus has only existed for a short time, meaning few studies on persistence have even been able to be conducted
3/ Second, have you noted all the cell types/body sites #COVID-19 can infect? (below). Have you obtained samples from all such sites in #LongCovid cases + searched for the #virus in a persistent form? (studies of cerebrospinal fluid, tissue biopsy etc?) nature.com/articles/s4159…
Read 6 tweets
14 Jul
Cool paper detailing what body sites, cell types, symptoms #COVID-19 has been connected to thus far 👉 But one thing: everyone knows that most persistent #viral (and #bacterial) pathogens are capable of #infecting/driving an equally extensive # of #symptoms, right?
2/ For example, in this interview, Dharam Ablashi (who co-discovered the #virus HHV6) explains how HHV6 has been shown capable of contributing to #cancers, type 1 #diabetes, Hashimoto’s, #MS, HPA-axis dysregulation, ME/CFS, Alzheimer’s, neuroinflammation..microbeminded.com/2020/06/28/int…
3/ ..and that the HHV6 can survive in
#microglia, astrocytes, macrophage, neurons/nerves, #pancreatic islet cells, the lung, gut epithelial cells, the #liver etc etc etc!
Read 6 tweets
2 Jul
So remember when I wrote this thread in an effort to explain why, coming from a mechanism of action perspective, #hydroxychloroquine (#HCQ) for #COVID-19 should be administered with #zinc?
2/ Well, this NYU preprint explains how the team performed a retrospective observational study to compare #hospital outcomes among patients who received #HCQ + azithromycin + #zinc vs. HCQ + azithromycin alone for COVID-19: medrxiv.org/content/10.110…
3/ They found that addition of #zinc sulfate to the #drug combo increased the frequency of patients being discharged home, and decreased the need for #ventilation, admission to the #ICU, and mortality or transfer to hospice for patients who were never admitted to the ICU.
Read 7 tweets

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