It’s nice to have a billionaire in your corner. Earlier this year, billionaire Vitalik Buterin pledged to devote $100 million to high-risk, high-reward COVID-19 efforts. He made good on at least $15 million of that when he jumpstarted The Long COVID Research Initiative.
Led on the science end by microbiologist Amy Proal, the effort also includes a former Google employee and product manager, Henry Scott-Green, an investor, Helga Gutmane, and startup founder Nick Harrold. That’s not your ordinary research foundation group – and these are not ordinary times.
TechCrunch reported Green has got hit hard enough by long COVID that he was unable to do even basic tasks. Green’s experience clearly lit a fire in his belly – he wants answers sooner rather than later.
Run through the PolyBio Research Foundation, the Long COVID Research Initiative (LCRI) effort looks like something that happens when Generation Z, with its focus on rapid development and agile programming, runs smack right into a traditional and slow-moving medical research system – and finds it wanting. The LCRI isn’t panning the usual medical research efforts – they’re want to do them faster.
“We’re running as a lean organization that prioritizes fast execution and close collaboration — and generally, and where it makes sense, trying to apply the organizational principles that have allowed tech to deliver big, ambitious projects quickly,” Scott-Green .
They hope to be the answer – or at least part of the answer – to the millions of shocked and angry long-COVID patients who expect their medical system to at least have something for them (welcome to the club). The Initiative even calls itself “A patient-driven movement to accelerate Long Covid Research”.
Lighting a Spark
The Initiative wants to quickly light a spark – and get the long-COVID field moving.
E. John Wherry, an immunologist at the University of Pennsylvania, told Science, “We need a spark, we need a philanthropic organization that has a risk tolerance much greater than NIH.” Of course – a spark – something that ignites the research world – is what the ME/CFS community has been looking for, and praying for, for years.
Eschewing the long lead times of federal efforts – grants can take a year or more to wind their way through the convoluted backwoods of the NIH – the group wants to function like a startup that balances “urgency with pragmatism”. The trick, of course, is how to do good science quickly.
That will take top scientists who can quickly pluck the wheat from the chaff and Proal – the lead scientist in the effort – has assembled a roster of respected scientists that hail from Harvard, Yale, Stanford, UCSF, Vanderbilt, Emory, and the J. Craig Venter Institute. Besides Proal and VanElzakker, some of the names – Systrom, Novak, and Iwasaki (recent keynote speaker at the IACFS/ME conference) – are familiar.
Viral Persistence Tagged
Viral persistence is “the trend we see the most evidence for.” Amy Proal
Instead of spreading itself thinly over the many areas of interest in the fast-growing long-COVID field, the LCRI appears to be doing a very smart thing – it’s throwing all its energy at this point on just one of them – viral persistence. Is the coronavirus – in one form or another – still present, and if it is, is it continuing to tweak the immune system in the long haulers?
You don’t spend $15 million to look for pathogens in the blood. This group is going to look in the tissues – something we’ve wanted to have happen in ME/CFS for a long, long time. If a pathogen or a piece of pathogen is putting the immune system on alert – which is then producing the symptoms in long COVID and/or ME/CFS – then finding a way to nail down that pathogen would be an immense step forward. No one has committed these kinds of resources to doing that. This is potentially a very big deal.
If the answer to the viral persistence question is yes, the Initiative plans to move into treatment trials that could include SARS-CoV-2 antivirals, immunomodulators, targeted anticoagulants, and microbiome-based therapeutics. If they get an answer for the SARS-CoV-2 virus, the next stop is the Epstein-Barr virus (EBV).
The group has already accomplished one of its main purposes – get the word out in a big way. The news of the new effort was quickly picked up by many major media outlets including Techcrunch, the Los Angeles Times, Yahoo News, Forbes, the Wall Street Journal, Science, and others. That’s good news for a group that hopes that their $15 million kickoff is just the start: it hopes to bring in $100 million over the next couple of years to dig deep into the molecular roots of long COVID.
Amy Proal – the Science Leader of the Effort on Long COVID Earlier This Year
The Disease That Shall Not Be – or At Least Is Not – Spoken?
The question of viral persistence has never gone away in that other post-infectious disease – you know – chronic fatigue syndrome (ME/CFS). Whether it’s enteroviruses or bits of enteroviruses, smoldering Epstein-Barr virus infections, or strange HHV-6 infections, researchers have proposed that all manners of pathogens may still be lurking somewhere. Nobody has had the money to really look for them outside of the blood.
Almost ten years ago, Michael Va Elzakker – one of the co-founders of the PolyBio Research Foundation – proposed in the Vagus Nerve Hypothesis that small infections found adjacent to the vagus nerve were tweaking it – producing the symptoms we see in ME/CFS. Now, we should be getting some answers to the viral persistence question – in long COVID, at least.
But what about ME/CFS and other post-infectious diseases? With four of its six projects featuring ME/CFS, the PolyBio Research Foundation that’s hosting the Long COVID Research Initiative has made ME/CFS a major emphasis. Amy Proal actually has ME/CFS, and in 2018 co-wrote a hypothesis paper proposing that “pathogen persistence” – the same topic the Long COVID Research Initiative is focused on – is driving it. Michael VanElzakker, of course, has been heavily invested in ME/CFS for the past ten years, yet I couldn’t find any mention of ME/CFS in the entire Long COVID Research Initiative website.
The fact that a group like PolyBio – which is so heavily invested in ME/CFS – chose not to mention it on the Long COVID Research Initiative should tell us something – and not something bad. Long COVID is where the interest and the money is. If you take as a given that much of long COVID is ME/CFS by another name, then what we really want is for the science on long COVID to move as quickly as possible. The faster it moves, the faster we move. If that’s true, why muddy the waters? Focus on long COVID – figure it out as quickly as possible – and open the door to ME/CFS.
Amy Proal, the originator of this effort wrote on Twitter:
“Our long-term vision is to iterate our collaborative infrastructure and cutting-edge technologies toward the study of viral and bacterial #pathogen activity in related conditions. These include #ME/CFS, #LongLyme, MS, and Alzheimer’s disease”.
That applies to private efforts like the Long COVID Research Alliance that are seeking to throw some lightning bolts into long-COVID research and “spark” some real interest – not to the big federal institutions like the NIH and CDC, whose job it is to support everyone who is ill. They can and should immediately plump up the ME/CFS research field so that it is able to digest the insights that are sure to come its way in the coming years. They’re the only ones with the resources to do that and that’s where we need to put our focus.
The 2 times I went into full remission for a couple of weeks (I have a 42-year journey with ME-CFS and believe me, full remission feels completely different from just having a good day) was due to treatment in a German clinic with IV Amantadine, daily for several weeks. After 4 days, the fog lifted each time, and slowly descended once I returned to the US. Amantadine pills did not ever work. I understand this treatment is not sustainable, as it is too toxic, but after these experiences, I knew that a persistent, smoldering virus (or viruses) was at the root of my illness.
I take oxymatrine in the form of Equilibrant for chronic enterovirus in the gut, and therefore no longer have regular bouts of coxsackie B. 3 tablets 2 x a day (and I had to start very small, 1/2 a tablet as the die-off is dreadful). I also use bactroban ointment daily in my sinuses to curb chronic sinus staph infections. I am on Famvir 500-1000mg daily to help with EBV. But, I still have high HHV-6 and EBV IGG titers, so know these viruses are active somewhere in my tissues. And though better overall, I do not feel normal and have to pace my activities to help with PEM.
I did have the good fortune to be studied by Michael Van Elzakker, and to be treated with Mestinon and a vagus nerve pacer, but neither was effective.
Am sharing all this in the hope that it’s helpful to the community.
Hi Maren, what does a “bout of coxsackie” look like? (I have IgG antibodies to it, but Equilibrant did nothing for me.)
Ray Peat has written about amantadine, used in Parkinson, has an anti-excitotoxic action.
I.e. – it’snot simply an anti-viral or rather, it’s mode of action in the body results in something that resolves a viral infection. Akin to a conversation in an earlier post about rapamycin and it’s many effects other than the one originally used/found for.
You could look up his article and get some clues what else you can do.
Good luck!
Thanks for poinitng this out:
Amantadine may indeed be a microglial inhibitor:
https://pubmed.ncbi.nlm.nih.gov/22035588/
Hi, Maren! We may be seeing some new and better EBV drugs coming out. With the EBV reactivation that’s been seen in long COVID I’ve been told interest in them is increasing. Let’s hope!
What new drugs for EBV reactivation ? New to The board. Thanks
J’ai fait des tests pour lyme et pour le bornavirus en Allemagne il y a 6 mois. Lyme et coinfections sont négatifs, mais le bornavirus est positif.Et d après le labo, il n’y a qu un seul traitement pour la maladie de Borna , c est l AMANTADINE. Le médicament me donne trop d effets secondaires, donc je ne sais pas si il est efficace dans cette maladie.
Encore un virus de plus activé dans mon corps…
I can add a tidbit here: Amantadine is used in a German Borna virus treatment protocol aimed at treating supposedly Borna virus related chronic illness. Borna virus is a largely animal-borne neurotropic virus. The Borna virus discussion has a controversial background similar to XMRV, with a scientist called Liv Bode warning against the virus polluting blood donations, but – if I recall correctly – established viral institutes did not regard it as pathological re. ongoing disease in humans and attributed some findings to lab contamination or non-standard lab methods, thus discontinuing research into it; then research was restarted after some deaths following Borna contaminated organ transplants demonstrated pathology in humans. In part of German alternative medicine, Borna virus is considered a possible cause of chronic fatigue syndrome, and the protocol aims at treating it with oral Amantadine (I believe it’s based on the assumption of persistent viral activity in the body).
Borna virus as a cause has never been accepted by established as a cause of chronic fatigue by established viral research in Germany, as I believe the view prevailed that either Borna virus in seldom cases gives humans fatal encephalitis, or it does not do anything to you (reminds of the binary “recovered or die” outcome expectations in the beginning of Covid pandemic).
I believe that because of the lab-contamination discussion and other concerns re. lab methods and reproducibility, (see e.g. https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(20)30379-0/fulltext ) Borna has never been proven beyond doubt to be linked to chronic fatigue syndrome; and there also seems to be controversy about whether positive effects of amantadine are related to its antiviral effects or rather other effects of it in the body.
But I can’t see why there should not be a probability for this neurotropic virus to induce a “Long Borna” condition when so many other viruses do, and when it has been established that Borna can cause encephalitis in humans.
Also, while the above-mentioned lancet reply states that “The well known, virus-independent effects of amantadine on Parkinson’s disease and other neurological conditions (…) undermine the hypothesis that it might improve depression through an antiviral mechanism”, I wonder how many neurological conditions may actually turn out to have an unknown viral component one day?
Anyway, the treatment protocol uses Amantadine; and I think Liv Bode continues to research Borna virus and amantadine in relation to psychiatric disease https://bmcpharmacoltoxicol.biomedcentral.com/articles/10.1186/s40360-020-0391-x .
Hello Maren,
What clinic are you talking about in Germany?
I live in the Netherlands so closeby and it might be interesting.
“That’s your ordinary research foundation group – and these are not ordinary times.”
Should this be “that’s NOT your ordinary research foundation group”?
🙂 Most definitely (lol). Thanks!
I don’t agree that leaving ME/CFS out of the wording is wise. This stigmatizes and erases ME/CFS. Long Covid clearly has at least a viral start, but many MEeps didn’t. My case, unlike classic viral ones, came on gradually without clear viral involvement.
Nothing about us without us.
Particularly in this case – where they are looking for viral persistence – I think it makes strategic sense since, as you point out, we don’t that everyone’s ME/CFS was caused by a virus or other pathogen, and we do know that quite a few pathogens do trigger it. It makes sense to me to focus on the apparently quite difficult work of finding out whether one virus is persisting somewhere in the body. If they can show that they’re able to do that – they can move onto EBV – probably the biggest trigger in ME/CFS.
Honestly, particularly in this kind of endeavor, I think this would be the way to go even if the funding wasn’t already totally tilted towards long COVID. Create the template and then apply it to other bugs.
An understandable point, however something that Covid has shown is how many asymptomatic infections there have been despite this being a novel virus, some of which have then given people long covid. It is quite possible that the supposedly non-infectious me/cfs cases are simply the result of asymptomatic infections. Secondly, virtually all me/cfs cases are characterised by immune dysregulation, even if the nature of it varies between individuals and there may be a variety of infectious triggers, also common with long covid.
Third, despite their best efforts, the psychiatric gaslighting brigade have failed to ‘own’ long covid, so may be it is best to power ahead on long covid and translate across to me/cfs in the fullness of time.
All great points Nigel.
Perhaps we could rename ME/CFS as
‘pre-covid dysregulation illness’.
Or
Pre-covid
Early
Warning
Sufferers
PEWS!
sorry, I can only read long covid, over and over again… On so many places. it hurts…we are ME/cfs with millions worldwide, so many in 25% group verry verry severe, so many commited suicide, so long ME/cfs excists together wit FM. for ME/cfs there are different triggers, not only infectious ones but the latest time you hardly read (research) on not infectous onset. There comes covid and yes, they are (verry) ill to, but how long and the big money comes, the research, the scientists, you name it… covid, covid, covid. but we have been suffering for decades tremendous and what is there for us? in the best case if there is for excample still an ongoing infection, they get treated, etc and MAYBE it opens the doors for the infectious ME group because there still would be tons of money and intrest wich is not or in the same case for FM. And the other ME/cfs onset groups stand/lay totally in the cold. It is as if there is suddenly no other onset then infectious ones for ME/cfs. For those, verry severelly affected ME/cfs patients, FM patients, you name it, who have seen over decades passing there lives and suffering severelly…this throwing with tons of money from all sides for such a short desease hurts. I even would not wonder if researchers from the ME/cfs comunity switch sides to long covid because of the name, the money, the problems with research for for excample ME/cfs they have (look at OMF, Nancy Klimas, so many …). Ofcource i do not want that the long covid patients suffer, I want them to be cured. But i want those tons of money and interest and researchers to for ME/cfs (every onset), FM, chronic lyme, etc We diserve it with our decades of suffering and neglect. Not even mentioning post covid vaccin desease…those who had bad luck…
Konijn, I echo your sentiments. Best case; covid spending and research will spill over to us/worst case; we will be overlooked again and relegated to continue our endless suffering. Where is the (big powerful) cavalry?
We are the cavalry really. We really have to push via advocacy to ensure that we have the funding to quickly incorporate the long COVID findings that are coming. Now is not the time to give up – now is the time to push harder.
Finally!!!! After of decades of negative standard blood tests revealing nothing, and most MECFS patients in the past being told “you are fine,” and sent home. Scientists are finally strenulously looking at virus reservoirs in tissues, the gut, etc.
Long COVID is very prevalent, very public, and has been zillions of research dollars. I, too, hate that pwMECFS have been ignored for years, but am glad money is finally being spent on diagnosing and treating chronic illness. This ‘spark’ will most certainly benefit us in the future. Hopefully sooner rather than later.
I remember when the NIH refused to fund any pathogen-related ME/CFS research -but now the coronavirus is so prevalent that viral research – and that will include antiviral treatments – including those for EBV – is now a big deal. I think that’s great news.
I think we just have to be patient (once again) Konjin. I can’t imagine that long COVID is not going to benefit people with a post-infectious disease. One good bit of news is that ME/cFS is well represented in the Commonalities section of the RECOVER project. (In fact, some people we are over represented.) Requests have been made from inside the RECOVER project to have ME/CFS cohorts. We have voices from inside the project advocating for us.
I do not think we will be forgotten. I do think we need to continue to push the feds, though to increase our funding and include us in the RECOVER project.
As maybe a bit of comfort, in her Twitter announcement https://twitter.com/microbeminded2/status/1567868860652572674?cxt=HHwWhMC-2f-amMIrAAAA Amy Proal said that “Our long-term vision is to iterate our collaborative infrastructure and cutting-edge technologies toward the study of viral and bacterial #pathogen activity in related conditions. These include #ME/CFS, #LongLyme, MS, and Alzheimer’s disease”.
The Forbes article reporting about the initiative said that ” Viral persistence is believed to be behind a number of other conditions including Myalgic encephalomyelitis, also known as ME or chronic fatigue syndrome, and multiple sclerosis (MS). (…) Though dedicated to working on Long Covid, Scott-Green said he hopes its model will one day be translated over to other chronic illnesses linked to infections. Hopefully Long Covid will be “the first domino in a series of breakthroughs,” he said.”
And on the Long Covid research initiative’s own website, in the section “Our Work” https://lc19.org/ourwork/ it states the intention to extend this research to related conditions incl. ME/CFS:
“The Big Picture: We stand at an important moment in time. Viruses beyond SARS-CoV-2 – such as Epstein-Barr Virus and the enteroviruses – are increasingly implicated in a growing number of chronic conditions, including ME/CFS, multiple sclerosis, Parkinson’s, and Alzheimer’s disease. Bacterial pathogens such as Borrelia burgdorferi (Lyme disease) are also increasingly connected to the development of chronic disease symptoms. Persistent viral or bacterial activity may even play a role in the human aging process, positioning this work at the center of longevity research. We will iterate the LCRI collaborative infrastructure and cutting-edge technologies toward the study of pathogen activity in these related conditions. This could usher in an era in which antivirals, immunotherapies, and related therapeutics become treatment possibilities for millions of patients across the globe.”
That’s a bold mission statment, so although current funding does go to LongCovid, it provides some hope to see ME/CFS on the agenda of the minds behind this initiative.
Thanks so much! I will put that quote in the blog 🙂
Agree. My trigger was double lumbar injections with Dexamethasone. EBV started within a Couple of days. one of my doctors Theorized it caused some sort of encephalitis. Anyway left me with CFS/ME, fibro and diabetes. I expected This for The Covid folks, especially where EBV was showing up in alot of Covid cases, and am glad That They Are researching a solution. Too many people’s lives are being ruined.
Great. Some billionaire gets the patents on any cure, and charges people $100000. How about governments fund research and make the results free for everybody. That is what government is supposed to do. When it is not subordinated to billionaires.
Since he gave the money to PolyBio to fund the project I don’t know why he or any other person who donates money to any cause really would benefit economically from it. You may not realize this but whatever PolyBio or any other private group can raise can’t begin to match the $1.15 billion in federal funding provided for long COVID research. So, basically we have both – pretty strong private and federal funding for long COVID.
One thing I didn’t mention is that some of the researchers associated with the Long COVID Research Initiative are also embedded in the RECOVER project – so the two projects should be able to talk to each other.
I’m excited to see what they find, and how quickly. I had a nasty bout of flu and then three years later ME/CFS seemed to kick in. At first I didn’t think it was connected, but in hindsight, symptoms were likely appearing in those intervening years. So for people like me who don’t really know if their onset was infectious, this could be helpful.
On a different note the DecodeME genetic study started this week – they’re hoping to recruit 25,000 people I believe!
Good to hear about DecodeME! 🙂
I am about to take up my offer to be part of DecodeME, about to fill in the questionnaire and practising salivating for the spit kit.They are asking for permission to access our medical records, BUT I do not think they will be very illuminating as most of my history is not digidtized. AND GPs notes are not very illuminating.
eg. after repeated tonsilitis infections, sinusitis infections and a nasty case of Mono where EVERYTHING was swollen, including my eyelids which I had great difficulty opening, my tonsils were touching each other pocked all over with yellow Strep lumps like BIG dimples on two golf balls and sticking to my epiglotis, 3-4 months later I had a tonsilectomy age 17 1972 , The surgeon was disgusted, I could hear him standing at the foot of my bed on the ward as I fought to escape the effects of the anaesthetic ” They were Disgusting, I had to dig them out.” I still have purple crescent shaped sore patches at the back sides of my throat. Numerous incidences of “Tonsilitis” followed, with “allergic” rashes to antibiotics : which I now understand are a sign of EBV infection.[ [ The Infection Game, Life is an arms race Dr Sarah Myhill & Craig Robinson, Table 18.4 p122 Dx Tonsillitis (Action) Notes: Be aware that Glandular Fever may present with tonsillitis. The Epstein Barr virus (EBV) is very good at switching on allergy and so antibiotics should be avoided or a nasty drug reaction may ensue { No Kidding} Indeed some doctors use this to dignose EBV because amoxicillin almost invariably produces a nasty rash.] My GP finally twigged and crossed out his next note of “Tonsilitis” and wrote “Sore Throat ” instead . And finally “?EBV” without any mention of this suspicion to me! None of this is available in my digital medical record. I had to pay to have it photocopied up to the beginning of the digitization, otherwise I would still be ignorant!!! None of the entries are ascribed to any GP author. Over & out for now
It certainly is , Cort . Great study and I just heard today I’m eligible for the second stage , which is DNA collection .
They are such great people running it , including PWME , and they’ve ensured it’s accessible to all , including those with severe M.E. CFS .
May not help me as I’m my late 60s but sure something will be found for future sufferers .
It does feel good to be doing something too 😊
This brought tears to my eyes. I feel really hopeful about this work. Seems like everything is coming together quickly and they’re looking to get to the root of the problem. Here’s to hoping they get some answers.
I’m sure that the RECOVER project is looking at viral persistence but this attempt to look for viruses in tissues other than the blood really seems unique to me. Just imagine if they find them in tissues but not the blood – and determine that the viruses in the tissues are sparking an immune reaction. that is contributing to or causing long COVID.
That changes everything we’ve assumed about viruses. It really seems like a potential game-changer to me. I hope they get their $100 million.
Exactly! Me too.
What does it mean that a virus is found in a tissue?
How can you know it is causing a problem?
I don’t think this is a straight-forward answer. A theory doesn’t mean it is so.
Aren’t Ron Davis and Robert Phair also looking for pathogens hiding in tissues other than the blood, or have I misunderstood? I think that they are hypothesising that a latent pathogen is keeping the Itaconate pathway turned on, causing the PEM in ME. I hope I’ve understood that right because many ME theories you read about don’t seem to hang together and it’s heartening when they do!
Long covid will be dismissed as a disease of the mind. Just like ME.
Largest genetic study of ME
https://www.bbc.com/news/uk-scotland-edinburgh-east-fife-62876472
With all due respect, but I think it’s going to be another failure. Because we are dealing with a heterogeneous disease.
But let me be wrong!
Leaving all people with Lyme borreliosis behind again and again and again. Any pathogen can cause disease and long term disease. It all depends on the ‘receptability’ of the host, co-factors and often co-infections of varous kinds. They need to look at pathogens!!! Viral, bacterial, parasites… How must long haulers with bacterial infections at play, feel themselves? Bring down those walls between the infectuous diseases and the answers may be found in the red thread between them. Hang in there everyone…
I would look at this way. They’re not leaving Lyme patients behind – they’re going full bore on long COVID patients. They really have no choice. Where else are you going to get $15 million to start off a $100 million campaign. Not in Lyme and not in ME/CFS but F they can crack the persistent pathogen issue in long COVID – of course diseases like post-treatment Lyme Disease and ME/CFS are next.
I fully undersand your cynicism. But I’m not sure ME is a heterogeneous disease. More and more self diagnosed symptoms are added on daily. One day, I believe, a diagnostic test will be found for a much more homogeneous group. And people who don’t meet the diagnosis will be in the horrid position of still needing further exploration.
I am not sure if studying “viral persistence” of SARS-CoV2 is enough to learn about postviral immune dysfunction in general. Of course, some exposure does trigger the cascade of events, but this exposure may be SARS-CoV-2, S1 protein, influenza virus, enteroviruses, and basically any “immunologically relevant event”. This comes with the crucial question: what´s the immune pathway(s) all these triggers feed into? In other words: what is the common biopathological denominator of ME/CFS? Long Covid has added to the many hints that this common denominator may be reactivation of EBV (and, possibly, other endogenous microbes). Hope they keep all their senses open to include this in their studies. I am sure they do 😉
The million-dollar question, Herbert:
if such a high percentage of the population has EBV, how come they don’t all have it get reactivated and get ME/CFs, if that is the theory?
From this perspective, is easy to think it is not the virus per se.
I think they will. They are going to look at the immune component. I don’t think it’s sufficient to find the pathogen, actually. It could be buried in the tissues but not causing any problem. They’re going to have to show pathogen persistence AND immune activation.
The ME/CFS field has been down this road already. Naviaux and Davies have clearly opined that anti-virals, long term anti-virals are not the way to go.
Naviaux’s cell danger theory predicates on this no longer being the initial insult, but hwo the body reaponded. Hecks, it’s Klimas’ model too.
I would keep an open mind. While these are clearly informed opinions, they’re opinions based on research in a disease that hasn’t gotten a lot of good research. Long COVID is getting more research and some of that is pointing an arrow at viral persistence. That’s why this group is devoting so much money to this topic.
If I understood some research on EBV and by Prusty on HHV6 correctly, I think the interesting thing is that researchers are starting to discover that viruses cannot only have pathological effects on the body when actively replicating and being accessible to antivirals (I think this called the lytic phase of the virus), but have developed very clever ways of hiding within the body while STILL interacting with the body and wreaking havoc (this I think is called “latent phase” of the virus). So I expect there is still a lot of amazing things to discover re. viral persistence also in ME/CFS.
Epigenetics at the Intersection of COVID-19 Risk and Environmental Chemical Exposures
https://link.springer.com/article/10.1007/s40572-022-00353-9
This overview of potential environmental contributors to Covid adds another dimension for researchers to consider.
If you are carrying a body burden of toxic chemicals (and according to the CDC, most of us are), all the viruses, bacteria, mycoplasma, fungi, etc. harbored in your body can reactivate when the chemicals are released from fat stores into the bloodstream.
Some of the ways body stores of chemicals can be released are sudden weight loss; aerobic exercise; severe stress; concurrent illness and ill conceived detoxification programs.
Very interesting!
What LCRI should be teaching us is that we need a MECFSRI to cut through the BS and concentrate funding and research on getting a biomarker/diagnostic test.
Our Nanoneedle has sat there unfunded since 2019. It’s an unharnessed weapon in this long war. And it’s not the only one.
We need to pick a top 5 from biomarkers based on criteria and get them funded for large N studies against other illnesses for specificity.
We need to get this done.
That’s the lesson.
Merci JR d’avoir clarifié ce que l’on sait sur le Bornavirus. J’en ai parlé à mon médecin, spécialiste d’EM/SFC.
Voici ce qu’il m’a répondu :” Les Bornavirus sont assez fréquents à population générale. Il y a quelques papiers dans la fin des années 90 qui ont montré une positivité de la sérologie de ces virus dans le syndrome de fatigue chronique surtout au Japon. Il n’y a pas par la suite eu d’autre article mettant en cause ce virus dans le ME/CFS . Comme tous virus il peut être le déclencheur du syndrome de fatigue chronique post infectieux sans en être la cause.”
Translate:
Thank you JR for clarifying what is known about Bornavirus. I talked to my doctor, an ME/CFS specialist.
Here’s what he said: “Bornaviruses are quite common in the general population. There are some papers in the late 90s that showed a positivity of the serology of these viruses in chronic fatigue syndrome especially in Japan. There was no further article implicating this virus in the ME/CFS. . Like any virus, it can be the trigger for post-infectious chronic fatigue syndrome without being the cause.”
Scheibenbogen found differences in underlying mechanisms between post-covid ME/CFS and ME/CFS
https://us02web.zoom.us/webinar/register/WN_fVEmlujiR3aD2IivJQI85Q
(…) Their findings also describe differences between post-COVID ME/CFS
patients and ME/CFS patients in the correlation between hand grip
strength and inflammatory biomarkers. This may indicate differences in
underlying mechanisms. The researchers’ findings have been published in
Nature Communications (…)
Webinar, Prof. Dr. Carmen Scheibenbogen
FM patients allowed to age out and tap out as usual. We’ll be reading these studies until we die or suicide. Have you ever seen an FM article with details like this…
https://www.pnas.org/doi/10.1073/pnas.2213524119
I share everyone’s frustration I can assure you, it is galling to see Long Covid getting the attention that ME/CFS should have received decades ago, and we’re still the poor relation it feels. On the other hand, and please don’t think me a member of what I call ‘the cult of positivity’, I do think there are more grounds now for cautious optimism than a few years back.
One of those is the advancement of technology. Up until very recently, researchers had to look painstakingly, and expensively, for just one thing at a time. With mass spectrometry (metabolomics, flow cytometry etc.) and the computing power to go with it, researchers can now run tests that are akin to saying ‘show me everything’. The costs are coming down and it’s got harder to ignore the (now) obvious way ME/CFS sufferers differ from the controls. Ditto long covid.
I also think the general direction of the science is now going our way. For example, viral and pathogen persistence, gut biome abnormalities, multi-factorial causation are not just the preserve of ME/CFS researchers, these are being actively investigated in may different areas, from cancer to neurological and autoimmune disorders. The simplistic one disease – one pathogen, the blood is the only place you need to look blah blah etc. is being replaced by a much more sophisticated understanding of disease aetiology. That can only be good news for us.
And also, essay nearly over, the pyschoquacks tried to ‘do an ME/CFS’ on long covid and failed. Even here in the UK the research money has gone to proper scientists. ME/CFS researchers are heavily involved in long covid and from what I’ve read those who are new to it are well aware of ME/CFS and the obvious link to it.
Hang on in there people, and good luck to everyone.
Thanks for pointing out the advancement in technology.
May I add to that the understanding of epigenetics that has been gained since I think the end of the 90s; it allows for understanding better how a genetic predisposition develops into a disease via interaction with environmental factors and immune events, and how the same genes can be “expressed” (i.e. translated into proteins) very differently.
And add to that the advent of bioengineering technologies like they were used for developing the Covid vaccine, or to engineer the recent Erlangen university lupus cure (CAR T-cell treatment) re. future treatment perspectives.
I agree I am glad there looking into long covid. Because when you get covid bad a lot people get really sick when they catch anything after that. I really don’t think it really goes away , it just stays dormant or something and then when you get a cold etc your body gets a really bad infection.