I can't remember what research has or has not been done it this area, so please excuse if I'm going over old ground. When a healthy person catches a virus, and then gets hit by what might be thought of as "normal" post viral fatigue, and then recovers thereafter, are the physiological mechanisms of that process understood by science? Can science explain what the physiological abnormalities are that cause that profound lack of energy in "normal" post viral fatigue? If science can explain that, then do we know if any of those same physiological abnormalities also exist in people with ME/CFS? Are people with ME/CFS stuck with those same physiological abnormalities that others are lucky enough to recover from? I appreciate a medical trial might typically examine the obvious comparison of people with ME/CFS against healthy controls. But what if ME/CFS participants were also compared against otherwise-healthy people suffering from "normal" post viral fatigue, and their biological abnormalities compared? Although I appreciate it would then need to control for whether the healthy subjects did in fact recover from their post viral fatigue within an expected timeframe.
There is very little research in this area and I don't think we have any real answers as to what post-viral fatigue is or if post-viral fatigue differs from ME/CFS. I suspect they are the same thing or closely related, since the symptoms are often very similar and there doesn't seem to be a definitive change from one state to the other that happens at any particular point. I guess the other way of looking at this might be: why do some people recover after a relatively short period and others don't? I think the Jason et al study on ME following mono might be the best we have.
Given that, until 2 years after covid hit, practically everyone in medicine, government, the media, and virtually every grouping apart from 'us' has point-blank denied that any disease does anything but kill people or is recovered from I would imagine the research base is rather small. The number of organisations that still proceed as if post viral stuff doesn't exist, no matter what they say, is remarkable.
Agree with what the two others have said. Technically most Long-Covid research is probably to a large extent just post-viral fatigue research (of course Covid-19 is still a very special virus) since a majority of the studies just ask patients how they are feeling at 4 weeks post-infection and then often don’t go beyond that. Many of those of course recover, but there's often no intricate analysis or long-term follow-up so you won't be able to say what is what. Scheibenbogen also published this study which is probably the closest research you’ll find to what you are looking for. Here she has two groups with ME/CFS similar symptoms (both fatigue and PEM have to be present) a couple months after Covid (3-8 months). Half of the patients go on to develop ME/CFS, the other half recover very slowly. There are some markers that she correlates to the development of ME/CFS rather than recovery, but it seems likely those might just be noisy factors.
I don't think researchers properly understand "sickness behaviour" either, and that's common and "everybody knows what that feels like". For that matter, they don't even know what "fatigue" is or how to measure it. No, they don't understand post-viral fatigue either. It is a bit surprising, since pharmaceutical companies would love to have a pill for treating fatigue, sickness behaviour, or other such very common symptoms. I don't get colds often, but I'd certainly like to have a "make the awful feelings go away" pill for that. To make such a pill, you need to understand the biological causes of those symptoms.
Sickness behaviour is not a symptom. It's a framework to infer disease, initially proposed by a veterinarian, if I recall correctly.
Wiki says: "Sickness behavior is a coordinated set of adaptive behavioral changes that develop in ill individuals during the course of an infection." To me, that fits the definition of "symptom", as defined in several dictionaries. A quick look showed several papers along the lines of "Specialized neurons that are activated after infection have been identified in the brain. These neurons orchestrate an array of sickness behaviours that help the body to cope with disease and to fight infection." Whether you consider sickness behaviour a symptom or a framework or a poetic construct, I'm sure there are plenty of people who would pay for a pill to reduce it or override it.
These already exist, in the form of 'flu' symptom reducers, and many other OTC medicines. In that they do nothing to fight the flu, in fact they reduce the symptoms of the immune system fighting it, AFAIK by interfering with aspects of the immune response, and possibly therefore prolong it
I just got over a flu. I refused to take NSAIDs because I felt that inflammation is important for fighting the infection. I read the label for Tylenol, and found that it is not anti-inflammatory, but it is antipyretic, so I didn't take that because fever is one of the immune system's weapons against infections. I would have appreciated a "wake me up when it's over" pill.
I certainly agree @Creekside that big pharma is missing a trick. If they could develop a pill to effectively get rid of 'sickness behaviour' symptoms they would be onto a billion dollar profit This must be a stupid question because surely someone must have thought of it, but since certainly for me at any rate PEM feels identical to flu plus other symtpms but the bodily experience is that of having an infection. I think thats true for many PwME. Is this an avenue thats being pursued? I mean are those neurons orchestrating symptoms in ME?
I certainly think it's likely. My initial ME symptoms felt identical to a flu starting up, except that they disappeared overnight. Now my baseline ME symptom constellation feels different from a flu, but they do share some characteristics. I do hope they study further these specialized neurons (and support glia). Is their activation a reliable marker of certain viral infections? Can they measure the severity of sickness behaviour by imaging those neurons? Are those neurons activated in PWME, possibly varying with PEM severity or overall ME severity? I think that's a more worthwhile study than most of what I've seen for ME research.
Behaviour is one step removed from symptoms. Why qualify "sickness" at all? Worse, why qualify it with anything to do with behaviour; it's BPS chum.
@Mij, I'm not particularly fond of the potential it introduces to undermining the need or want for patient reporting. It's interpretive BEYOND the mangling of what can be done via questionnaires. Sorry, I'm mangling my words. It imo introduces an unnecessary third party risk, if that makes any sense. But I appreciate the concept, and how it encapsulates many symptoms into a easy-to-digest thing.
Ah, but I'm not suggesting that the neural imaging should qualify something; I'm suggesting that it should quantify it. Animal grooming is quantifiable: you can statistically measure the frequency of it, and maybe how many licks per head movement. That's a measurable factor of neural function. If you can correlate that with the activation of specific neurons, you can pose hypotheses and test them, with mathematical reliability. That's quite different from questionnaires whose results depends on how you word it and interpret it. The BPS types will always be there, twisting words for their benefit. If you develop a neuroscience based on quantifiable measurements of specific brain cells and symptoms or behaviours, the experts who use only qualified data might be easier to ignore. "Where's your supporting quantified data?"
