News about Long Covid including its relationship to ME/CFS 2020 to 2021

[leokitten]

I’m wondering whether some or all of the “feels different to ME” comments may come from people who have or had ME. Still doesn’t convince me as those who had ME and then got Covid but didn’t feel much different would likely have not taken part in the study; they may even never have had a Covid test if the symptoms seemed similar to an ME relapse.

The problem too is that everyone with long COVID is still in their first year of the post viral syndrome stage. My ME symptoms and overall experience were so different in the first year than the years that followed, and it feels so completely different now than it did then. The disease evolves and changes. It makes for a false comparison unless you ask people with viral triggered ME in their first year to compare it to long COVID in the first year.

 

[rvallee]

The problem too is that everyone with long COVID is still in their first year of the post viral syndrome stage. My ME symptoms and overall experience were so different in the first year than the years that followed, and it feels so completely different now than it did then. The disease evolves and changes. It makes for a false comparison unless you ask people with viral triggered ME in their first year to compare it to long COVID in the first year.

Loud and clear. I did not have significant fatigue until years later. Before and in that time I did have mild fatigue but absolutely nothing that compares. And even then it never was a defining symptom, hence why comparisons to "chronic fatigue" completely fail.

But it is telling, that in a scientific paper they choose to separate two highly similar conditions, a question of major importance and deserving of careful consideration, because of... feelings. Even literally stating so. Just that. Feelings. And this passed peer review. Frankly peer review in medicine is a complete joke. Strict in some aspects but on others anything goes.

So have we now entered the era of feelings-based medicine? Not that it's new but that it's becoming a norm. Let's skip real trials and just go with the feelings of self-proclaimed experts, is something currently actually argued in a major medical journal. That's feelings. Because that's also about the argument given in the NICE LC guidelines as well, they felt ME was out of scope. Because feelings. None argued, or even stated. It just feels out of scope because it feels out of scope and nobody wants the stink of "chronic fatigue" so let's... leave us mistreated, I guess? Yeah that oughta solve everything. Let's keep the conditions in place that led to COVID long haulers to be dismissed the usual way yet again, guaranteeing its continuation in the future if there's ever the tiniest hint of a feeling that it's different.

Not only is medicine regressing, the regression is accelerating. At least in the chronic illness space. Acute medicine is doing amazing. Oh, chronic medicine, why can't you be more like acute medicine, competent, responsive AND scientific?

 

[Kalliope]

The Wall Street Journal - Experimental Drugs Aim to Treat Long-Haul Covid Patients

Leronlimab, a monoclonal antibody administered through subcutaneous injections, was developed as an HIV drug. When the pandemic hit, the company shifted to Covid-19. The same receptor that allows HIV to enter cells is also important in regulating immune cells; som doctors believe long-term Covid symptoms are caused by the immune system going haywire.
...
"We are hopeful we can control the neuroinflammation in the brain which we think causes a lot of these problems with autonomic dysfunction, fatigue, brain fog," says Dr. Kelly.
...
Organicell, a Miami-based biotechnology company, is looking at testing Zofin, an experimental drug tested for chronic obstructive pulmonary disease, or COPD, on long Covid patients. Zofin uses nanoparticles to reduce inflammation and microRNA to target different genes.
...
Some doctors believe that some long-haul Covid patients are suffering from myalgic encephalomyelitis/chronic fatigue syndrome, a post-viral condition. AIM ImmunoTech, an Ocala, Fla., biotechnology company, recently got approval to expand its ongoing clinical trial for CFS to include Covid patients who have chronic fatigue-like symptoms, says Tom Equels, CEO of the company. The company is treating patients with Ampligen, an experimental antiviral drug administered as an IV infusion.

 

[Helene]

I expected nothing better from Greenhalgh, it's still disappointing that they did not bother to learn a damn thing, still anchored on the invalid definition of ME as fatigue, THE fatigue. Nevermind that they say the same things for the same reasons and would explain the exact same way that LC is not just fatigue if one suggested so. Nevermind that it isn't really relevant what people "feel" is the cause of fatigue, even less so that it's a common thing to say for pwME that it an extreme level of fatigue unlike any normal fatigue, let alone that it's far far more than just that or even that PEM is obviously not the same as fatigue itself, even the extreme kind. Nevermind that dysautonomia causes fatigue and that it's very common in both. Nevermind it all. It's frankly getting silly, the level of willful ignorance, but that's just par for the course with us, we are not deserving of people actually being bothered by such things as facts like they normally do.

This paragraph is insulting. It was probably meant to be. Very silly to piss on our faces when all it does is splash back at them. It's entirely out of ignorance but it's still frustrating, as it's all coming at a time when it could have tipped the entire issue towards future progress given the NICE committee and whatever Cochrane is doing in the meantime waiting for others to absolve them of any responsibility in making a decision that will displease people irrelevant to the issue. Instead everything is stalemating. What a dumpster fire.

I browsed a bit. Of course if you'd remove the labels and context this may as well be an ME study. The statements and facts are the same. There is no mention of pacing, only one reference to exertion increasing symptoms, but as they did not bother to read anything about ME, of course they have no clue about PEM and since they shut the door on us they shut the door on this as well. Dumb dumb dumb and self-defeating.

I knew Greenhalgh would stab us in the face. Really silly that she and her team do not realize that in so off-handedly stabbing us without even looking back, they are also stabbing the LC in the back. Crabs in a bucket mentality meets escalation of commitment aligning to repeat the exact same mistakes for the exact same reasons. Frankly things are moving backwards right now, for everyone.

And nitpicky but one does not "express empathy". One either feels or has empathy and one expresses sympathy. Whatever.

Sometimes I wish there was a "Really like" button.

 

[Dolphin]

Some doctors believe that some long-haul Covid patients are suffering from myalgic encephalomyelitis/chronic fatigue syndrome, a post-viral condition. AIM ImmunoTech, an Ocala, Fla., biotechnology company, recently got approval to expand its ongoing clinical trial for CFS to include Covid patients who have chronic fatigue-like symptoms, says Tom Equels, CEO of the company. The company is treating patients with Ampligen, an experimental antiviral drug administered as an IV infusion.

That might sound impressive to investors but I believe the trial is just open label, uncontrolled clinical care with maybe 100 (?) patients. My guess is not many long haulers will take part.

 

[Sly Saint]

"We are hopeful we can control the neuroinflammation in the brain which we think causes a lot of these problems with autonomic dysfunction, fatigue, brain fog,"

it's funny how this keeps coming up as an explanation for symptoms like brainfog, and yet one of the main objections by some to using ME as a name was because they said there was no neuroinflammation.

How are they now able to say it's what is causing the problems for covid-19 patients?

 

[rvallee]

Australian study finds COVID-19 'long haulers' suffer symptoms months after coronavirus infection

https://www.abc.net.au/news/2020-12-23/long-term-effects-of-covid-study-in-medical-journal/13007498


Not much new but posting because:

Dr Charles said international research put the proportion of COVID-19 patients who became "long haulers" at between 2 and 10 per cent of cases.

"Given that we've had this 26,000 cases, we're probably looking at hundreds of cases here in Australia," he said.

He said patients could gradually build up their strength with physiotherapy and exercise, but it had to be gradual.

"It appears that once you overdo it, it really does cause you to go backwards," he said.

The longer our BPS overlords and their enablers dig in their heels and their nonsense remains perceived wisdom, in places like NICE and Cochrane the inaptly named Up-to-date or Mayo, the more people will continue to be hurt by ignorance. Because for most of those, especially things like the Cochrane review on exercise, all the framing is on fatigue. These people do have fatigue, therefore it applies.

At least now the second part, the payback, is acknowledged. Only in this specific case, though. Why for them and never for us? Who the hell knows, when you pick and choose evidence nothing matters. That's about the smallest bit of progress that can possibly be made, a quantum packet of begrudging progress.

 

[rvallee]

The Mysterious Link Between COVID-19 and Sleep

https://www.theatlantic.com/health/archive/2020/12/covid-19-sleep-pandemic-zzzz/617454/

Missed this because the focus seemed to be only on sleep but it has some good bits:

By contrast, the post-COVID-19 patterns are sporadic, not clearly autoimmune in nature, says Venkatesan. The symptoms can appear even after a mild case of COVID-19, and timescales vary. “We’ve seen a number of patients who were not even hospitalized, and felt much better for weeks, before worsening,” Venkatesan says.

Glad some people are finally seeing this pattern. About damn time.

Still, she believes, symptoms are most likely due to inflammation. Indeed, the leading theory to explain how a virus can cause such a wide variety of neurologic symptoms over a variety of timescales comes down to haphazard inflammation—less a targeted attack than an indiscriminate brawl. This effect is seen in a condition known as myalgic encephalomyelitis, sometimes called chronic fatigue syndrome. The diagnosis encompasses myriad potential symptoms, and likely involves multiple types of cellular injury or miscommunication. In some cases, damage comes from prolonged, low-level oxygen deprivation (as after severe pneumonia). In others, the damage to nerve-cell communication could come by way of inflammatory processes that directly tweak the functioning of our neural grids.

The unpredictability of this disease process—how, and how widely, it will play out in the longer term, and what to do about it—poses unique challenges in this already-uncertain pandemic. Myalgic encephalomyelitis is poorly understood, stigmatized, and widely misrepresented. Medical treatments and diagnostic approaches are unreliable. General inflammatory states rarely respond to a single prescription or procedure, but demand more holistic, ongoing interventions to bring the immune system back to equilibrium and keep it there. The medical system is not geared toward such approaches.

I would say discriminated is more accurate than stigmatized but still, good to see it clearly.

A central function of sleep is maintaining proper channels of cellular communication in the brain. Sleep is sometimes likened to a sort of anti-inflammatory cleansing process; it removes waste products that accumulate during a day of firing. Without sleep, those by-products accumulate and impair communication (just as seems to be happening in some people with post-COVID-19 encephalomyelitis). “In the early stages of COVID-19, you feel extremely tired,” says Michelle Miller, a sleep-medicine professor at the University of Warwick in the U.K. Essentially, your body is telling you it needs sleep. But as the infection goes on, Miller explains, people find that they often can’t sleep, and the problems with communication compound one another.

 

[rvallee]

It's getting weird living in a world in which those 2 things are true:

1. Medical professionals reject the ME name because there is no evidence of neuroinflammation
2. A sober look at the evidence, detached from the manufactured controversy, almost always leads to the conclusion of: wow this really looks a lot like neuroinflammation if only we could confirm the evidence

No guarantee it's that. It's just that it really looks a lot like the best possible explanation. Which was always the basis. Hence the incessant requests for decades to study this.

Amazing doublethink. Different context, I guess, going from disbelief over how our symptoms, insisting they can't possibly be real and therefore not worth looking, over accepting it is believable in this case because the symptoms are at least somewhat believed.

 

[Jonathan Edwards]

A sober look at the evidence, detached from the manufactured controversy, almost always leads to the conclusion of: wow this really looks a lot like neuroinflammation if only we could confirm the evidence

I am not aware of this ever being a sober look orbiting detached. It is just chucking out another buzzword. I think the situation is clear - there is no evidence of brain inflammation. And the clinical picture does not even suggest it.

I am not sure there is so much doublethink here as different people wanting to prove different beliefs.

 

[Mij]

it's funny how this keeps coming up as an explanation for symptoms like brainfog, and yet one of the main objections by some to using ME as a name was because they said there was no neuroinflammation.

How are they now able to say it's what is causing the problems for covid-19 patients?

Because that's what he 'believes and "thinks" is occuring:

Dr. Kelly says they believe leronlimab may be alleviating brain inflammation. Leronlimab binds to a cell receptor that contributes to the regulation of immune cells that sometimes flood an area and destroy tissue. Blocking that receptor may slow down the inflammatory response, which some scientists believe is triggering problems in long Covid patients.

“We are hopeful we can control the neuroinflammation in the brain which we think causes a lot of these problems with autonomic dysfunction, fatigue, brain fog,” says Dr. Kelly. The company says patients haven’t reported significant side effects in the clinical trials they’ve done for Covid and HIV. Dr. Kelly says the interest in such a treatment is tremendous. “I get emails every day about wanting to participate in the trial,” he says.

 

[rvallee]

I am not aware of this ever being a sober look orbiting detached. It is just chucking out another buzzword. I think the situation is clear - there is no evidence of brain inflammation. And the clinical picture does not even suggest it.

Then lots of neurologists are throwing buzzwords, independently. Which may be true, but I've lost count of neurologists saying they suspect this is the most likely cause. If it's wrong it's wrong, it's just the contradiction of this being often stated as a promising hypothesis when looking at similar cases while being soundly rejected as being possible at all with us that is comical. Very similar to the odd conflict of there being multiple post-XXX syndromes but somehow the idea of there being a post-infectious illness phenomenon being silly. Weird twisted logic.

There's no convincing evidence yet that leads to a credible cause. There usually isn't until there is, though. Pretty much by definition, the explanation of the cause here will defy medical science and have no evidence, if it didn't we'd already know about it.

 

[rvallee]

High rate of persistent symptoms up to 4 months after community and hospital-managed SARS-CoV-2 infection

https://www.mja.com.au/journal/2020...ter-community-and-hospital-managed-sars-cov-2

In Australia. Pre-print.

Recovery after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection remains uncertain. A considerable proportion of patients experience persistent symptoms after SARS-CoV-2 infection which impacts health-related quality of life and physical function. Multi-disciplinary follow-up is recommended for patients with post-COVID illness and to assess health-related quality of life and physical function.

Between April and June 2020, 78 individuals were enrolled, of whom 69 were managed in the community (30 mild, 39 moderate and 9 hospitalised

The most common reported initial COVID-19 symptoms were fatigue in 62, cough in 50, and headache in 44 individuals. At median 69 days after diagnosis (IQR 64-83), 31 patients had persistent symptoms including fatigue in 17, shortness of breath in 15 and chest tightness in 4, including 7 hospitalised and 24 community-managed individuals

Although more common following severe illness, 35% community-managed patients within ADAPT have persistent symptoms several months post infection

 

[rvallee]

High rate of persistent symptoms up to 4 months after community and hospital-managed SARS-CoV-2 infection

https://www.mja.com.au/journal/2020...ter-community-and-hospital-managed-sars-cov-2

In Australia. Pre-print.

This was covered in Australian news and:

 

[Tom Kindlon]

 

[rvallee]

Haven't watched, 28 min. Will try tonight. From Germany.

 

[rvallee]

Looked liked yet another annoying rehabilitation study at first



But upon closer look it seems like they adapted to feedback and understood that figuring out why rehabilitation is not happening is more important than trying to mash it into shape.



Even took material from the ME clinicians coalition, I think the first sighting I have seen in the wild. Encouraging, they seem to understand PEM well enough to provide a safe study.





Local researchers from Quebec City so I pointed them in the direction of Moreau's team. Fingers crossed.

 

[rvallee]

Neurological Manifestations of COVID-19 Feature T Cell Exhaustion and Dedifferentiated Monocytes in Cerebrospinal Fluid

https://www.cell.com/immunity/fulltext/S1074-7613(20)30539-2

• Single-cell atlas of cerebrospinal fluid in Neuro-COVID and controls
• Expansion of dedifferentiated monocytes and exhausted CD4+ T cells in Neuro-COVID
• Less pronounced interferon signature in Neuro-COVID than in viral encephalitis
• Curtailed interferon-response in severe Neuro-COVID

One thing that's been noted is that severe patients, in the ICU severity sense, experience more numerous and more intense neurological symptoms. Another thing is one notable factor in Long Covid appears to be number of symptoms at onset, especially neurological. Many arrows pointing in the same direction.

Patients suffering from Coronavirus disease 2019 (COVID-19) can develop neurological sequelae, such as headache, neuroinflammatory or cerebrovascular disease. These conditions - here termed Neuro-COVID - are more frequent in patients with severe COVID-19. To understand the etiology of these neurological sequelae, we utilized single-cell sequencing and examined the immune cell profiles from the cerebrospinal fluid (CSF) of Neuro-COVID patients compared to patients with non-inflammatory and autoimmune neurological diseases or with viral encephalitis. The CSF of Neuro-COVID patients exhibited an expansion of dedifferentiated monocytes and of exhausted CD4+ T cells. Neuro-COVID CSF leukocytes featured an enriched interferon signature; however, this was less pronounced than in viral encephalitis. Repertoire analysis revealed broad clonal T cell expansion and curtailed interferon response in severe compared to mild Neuro-COVID patients. Collectively, our findings document the CSF immune compartment in Neuro-COVID patients and suggest compromised antiviral responses in this setting.

 

[Helene]

Looked liked yet another annoying rehabilitation study at first



But upon closer look it seems like they adapted to feedback and understood that figuring out why rehabilitation is not happening is more important than trying to mash it into shape.



Even took material from the ME clinicians coalition, I think the first sighting I have seen in the wild. Encouraging, they seem to understand PEM well enough to provide a safe study.





Local researchers from Quebec City so I pointed them in the direction of Moreau's team. Fingers crossed.

Good work rvallee!

 

[Tom Kindlon]

https://nsuworks.nova.edu/grant_awards/24/