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..
4/ “...and also #ME/CFS, a condition which has long been speculated to have infectious origins although some scientists feel there could be a range of potential causes, and bears a number of similarities to long Covid.
5/ "The phenomenon of people developing chronic symptoms after an infectious #outbreak is not new," she says. "If the Sars-CoV-2 #virus didn't do this, it would pretty much be the only documented time where a major pathogen didn't result in chronic cases.
6/ There's a huge amount of studies, which have been neglected by the mainstream medical community, showing how infectious #organisms can persist in tissue, and contribute to disease processes...
7/ ...Some viruses are highly neurotrophic, meaning they can burrow into #nerves, and hide out there, and there's evidence that Sars-CoV-2 is capable of this."
8/ Proal says that in the past, many doctors have been quick to attribute post-infectious syndromes to psychological factors, rather than the latent effects of a #pathogen still causing harm somewhere in the body.
9/ However over the past decade, outbreaks of #Ebola, Zika, and now Covid-19 have all resulted in long-term chronic #illness in a proportion of survivors, resulting in an increased openness to this idea.
10/ But in another sub-group of patients, something even stranger may be happening. A number of studies have reported reactivation of the herpes zoster virus – most commonly known as the cause of chickenpox – as well as the Epstein-Barr virus, and cytomegalovirus in...
11/ ... acute Covid-19 patients. These are all #viruses that are known to be retained in the body for life as they can remain inactive inside cells...
12/ Some researchers have speculated that Covid-19 could be triggering the reactivation of #viruses that have lain dormant in the body for years or even decades, leading to the development of #chronic symptoms.
13/ "One of the things that the Sars-CoV-2 virus does, is it blunts interferon signaling, and interferons are part of the immune system which keeps viruses in check," says Proal.
14/ "So, if you already had the Epstein-Barr virus lying dormant in your body, it might then reactivate, and infect a new nerve or new tissue, maybe get into the central nervous system, and that could result in these chronic symptoms."
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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)
It was inspiring to virtually attend the first Inaugural Robert D. Moir Symposium this past Friday. Rob was a friend and constant source of inspiration, plus an amazing sounding board for novel ideas. He passed away from glioblastoma one year ago today.
2/ Like most great scientists I’ve known, Rob was not content to study just the presence or absence of compounds/organisms in the human body. Instead his thinking continually gravitated towards the vital question of “what are they DOING??”
3/ Via that lens - the constant question of “why?” and a passion for characterizing the molecular biology of the “why?”...Rob uncovered that amyloid in the #Alzhiemer’s brain has a function (it appears to act as an antimicrobial peptide)
1/ This excellent study by @aaronmring/@VirusesImmunity and team found that COVID-19 patients exhibit dramatic increases in the production of antibodies against thousands of human extracellular and secreted proteins (the exoproteome) compared to controls 👇
2/ The million dollar question is: what molecular mechanisms underly this antibody/#autoantibody production? It is worth interpreting the findings via the lens of human #microbiome/#virome activity + the activity of persistent pathogens (such as EBV) harbored by study subjects.
3/ Every study subject harbored extensive microbiome/virome communities comprised of trillions of organisms during #COVID-19 infection…with such ecosystems now understood to persist beyond just the gut but also in other body sites (#lung, liver etc).
Important paper 👉 A team in Tokyo took RNA-seq data from the Genomic-#Tissue Expression Project: a public resource created to study tissue-specific gene expression/regulation from 54 tissue types collected from 1000+ healthy individuals at autopsy: bmcbiol.biomedcentral.com/articles/10.11…
2/ They successfully identified 39 viral species in at least one tissue (tissue types included #brain, pituitary, esophagus, thyroid, #heart, breast, lung, kidney, adrenal gland, prostate, #nerve, adipose tissue, blood vessel, ovary, uterus etc)
3/ Viruses identified in the various tissue samples included EBV, HSV-1, Varicella, CMV, HHV6-A/B, HHV-7, HCV, HPV, adeno-associated virus...and 16 RNA #viruses including Respiratory syncytial virus (RSV), Parainfluenza Virus 3..