Viral Titers--A statement by Robert Naviaux

[frozenborderline]

Many illnesses display metabolomic changes, but these changes are not viewed as causal.

Naviaux has essentially stated in so many words that he doesn't know exactly what has explained the metabolic changes... He never said they're causal, however he did the most detailed and broad data-collection of any researcher so far. Really, what issue do you take with his theory?

People have expanded on his theory later to discuss how purinergic signalling could mediate these changes and how the feedback loops involved in extracellular atp and purinergic signalling could work in CFS, but that was all speculative work. It doesn't make naviaux's work any less valid

 

[msf]

He's addressing viruses because it's a common issue in CFS, at least as a trigger. He can't provide a condensation of every possible cfs trigger every time he discusses a specific issue. That makes no sense

Hmm, don´t think we are going to go anywhere here.

 

[msf]

With the pathogen theory of ME/CFS, the thing to consider is whether the presence of certain pathogens in the body is a necessary or a sufficient condition to cause ME/CFS.

If we look at the enterovirus research on stomach and muscle tissues biopsies, ME/CFS patients were much more frequently found to have enterovirus infection in these tissues; but these enterovirus tissue infections were also found in healthy controls.

So that suggest that enterovirus infection in the muscles or stomach is not a sufficient condition for developing ME/CFS (ie, on its own, enterovirus infection in these tissues is not sufficient to cause ME/CFS, which we know from the fact that healthy controls also have the same infections).

And that implies that some other factor (some immunological factor perhaps) must also be present before these chronic enterovirus infections can cause ME/CFS. Possibly that factor may be what Naviaux's line of research will find.



That being said, if you look at the enterovirus research on brain biopsies in ME/CFS, although there have only been 3 such brain biopsies, all 3 found enterovirus infection in the brain, whereas none of the 8 controls had this infection. So there is a 1 to 1 correspondence with who has chronic enterovirus brain infection, and who has ME/CFS.

Of course with only 3 brain biopsies, there is not yet much statistical significance to this finding; but so far at least, the brain biopsy research does suggest that cerebral enterovirus infection is on its own a sufficient condition to cause ME/CFS.

Wow, someone using pathogen instead of virus! Give Hip a nobel prize!

 

[Hip]

Wow, someone using pathogen instead of virus!

There are some non-viral pathogens linked to ME/CFS, but nearly all the data we have about pathogen involvement relates to viruses.

The only non-viral pathogens linked to ME/CFS in studies are the bacterium Chlamydia pneumoniae, the Q fever bacterium Coxiella burnetii (but that's rare), and the protozoan parasite Giardia lamblia. You can also include Borrelia if you consider chronic Lyme as a form of ME/CFS.

There are other pathogens such as Mycoplasma, Bartonella, Babesia and Brucella that are found in ME/CFS patients, but these are usually considered co-infections that may worsen the condition, rather than pathogens that can cause ME/CFS on their own.

Interestingly though, Dr Lerner's antiviral studies found that when ME/CFS patients have active herpesvirus infections along with such bacterial or protozoal co-infections, the antiviral treatment did not work as well as it did in patients with just pure viral infections and no co-infections.

 

[duncan]

There may be a little bit of inadvertent definitional circular reasoning or cannibalization going on. (Can't think of the right wording to describe it.)

If ME/CFS is NOT immune dysfunction of some sort, or perpetual automimmune response, both or either triggered by exposure to an infection, then aren't we talking about an infection ongoing, just unrecognized? Then wouldn't the appropriate diagnosis be an enterovirus or a herpes relative or Lyme or Babesia that is chronic, simply at subclinical levels not typically or usually picked up or recognized by standard diagnostic protocols?

So this is to say, ME/CFS would be simply a label for a cluster of similar symptoms generated by disparate diseases. Accordingly, the appropriate label would be the respective diseases themselves, yes?

But if each of these pathogens is truly resolved, and the symptoms manifested are due to immune dysfunction or autoimmune response, then a label of ME/CFS as a distinct entity would seem appropriate.

 

[msf]

There are some non-viral pathogens linked to ME/CFS, but nearly all the data we have about pathogen involvement relates to viruses.

The only non-viral pathogens linked to ME/CFS in studies are the bacterium Chlamydia pneumoniae, the Q fever bacterium Coxiella burnetii (but that's rare), and the protozoan parasite Giardia lamblia. You can also include Borrelia if you consider chronic Lyme as a form of ME/CFS.

There are other pathogens such as Mycoplasma, Bartonella, Babesia and Brucella that are found in ME/CFS patients, but these are usually considered co-infections that may worsen the condition, rather than pathogens that can cause ME/CFS on their own.

Interestingly though, Dr Lerner's antiviral studies found that when ME/CFS patients have active herpesvirus infections along with such bacterial or protozoal co-infections, the antiviral treatment did not work as well as it did in patients with just pure viral infections and no co-infections.

A good summary, but I think it should be pointed out that the q fever and giardia cases seem to be better established than any particular virus in terms of them being a trigger. That may be a result of the fact that the viruses that are suspected are more common than either of the above pathogens, but it would still seem to suggest that either of those infections would be a better bet if you wanted to establish how a particular trigger leads to me, assuming, that is, that naviaux's hypothesis of multiple triggers leading to one condition holds.

 

[Hip]

q fever and giardia cases seem to be better established than any particular virus in terms of them being a trigger.

Epstein-Barr virus is also well established as a trigger, as several studies have shown that around 1 in 10 patients who have mononucleosis will go on to get ME/CFS.

it would still seem to suggest that either of those infections would be a better bet if you wanted to establish how a particular trigger leads to me

They would certainly be worth studying more, to see if they can shed light on the mechanisms of ME/CFS.


Dr Jonanthan Kerr had the idea of studying parvovirus ME/CFS to see if this could shed more light on the mechanisms of ME/CFS in general.

Parvovirus ME/CFS is quite unique, in that it is the only form of ME/CFS in which there is a classic and obvious chronic viral infection in the blood. Parvovirus ME/CFS is caused by a normal ongoing viral infection, with lots of viral particles to be found in the blood, which explains why you feel sick.

Whereas with enterovirus and herpesvirus ME/CFS, there is no classic chronic viral infection to be found in the blood (which is why blood PCR is often negative). The enterovirus and herpesvirus infections in ME/CFS are more mysterious. In the case of enterovirus ME/CFS, we know that this virus is hidden inside cells a chronic non-cytolytic intracellular infection.

That's why lots of people doubt the viral hypothesis of ME/CFS in the case of enterovirus and herpesvirus, because blood PCR will often be negative, so skeptics say: "where's the infection?"

But with parvovirus ME/CFS, nobody doubts that a viral infection causes it, because that infection is obvious to see.

 

[duncan]

Parvovirus ME/CFS is quite unique, in that it is the only form of ME/CFS in which there is a classic and obvious chronic viral infection in the blood.

Then that patient with symptoms that match broad ME/CFS symptoms has a parvovirus. Why even bother with the ME/CFS label?

This matters as efforts to treat should ultimately be tied back to the cause, in this case an acknowledged pathogen.

I think this holds true with all cases which can be demonstrated to be ongoing infections.

 

[frozenborderline]

There may be a little bit of inadvertent definitional circular reasoning or cannibalization going on. (Can't think of the right wording to describe it.)

If ME/CFS is NOT immune dysfunction of some sort, or perpetual automimmune response, both or either triggered by exposure to an infection, then aren't we talking about an infection ongoing, just unrecognized? Then wouldn't the appropriate diagnosis be an enterovirus or a herpes relative or Lyme or Babesia that is chronic, simply at subclinical levels not typically or usually picked up or recognized by standard diagnostic protocols?

So this is to say, ME/CFS would be simply a label for a cluster of similar symptoms generated by disparate diseases. Accordingly, the appropriate label would be the respective diseases themselves, yes?

But if each of these pathogens is truly resolved, and the symptoms manifested are due to immune dysfunction or autoimmune response, then a label of ME/CFS as a distinct entity would seem appropriate.

But ME/CFS is almost certainly a complex metabolic/autoimmune response to pathogens/stressors/etc... That doesn't at all mean that there can't also be low-level viral infections, although I don't think the data on that is as robust as the data on metabolic/immune disturbances. But healthy people have some of these same viruses ongoing all the time. therefore the response should be more on what differs from healthy people in how our bodies respond to these viruses. I should say that i'm on antivirals while also being skeptical of them. I need to work with and not piss off my cfs doctor, so I will at least try them. but i've been only getting worse while on them. I am more looking forward to IVIG and thyroid supplementation as I am more confident in treating the immune/metabolic abnormalities than I am in treating the pathogens directly. Lyme triggered my CFS but i'm not on antibiotics. i have found the chronic lyme community toxic in some ways. yes, there is some evidence that suggests borrelia can survive a standard course of antibiotics, but everywhere i look in the chronic lyme community, people are on years-long IV antibiotic courses with no way to measure whether the infection is gone or not (because they don't trust the standard tests, maybe for good reason) and they don't generally seem to be improving much. If there is improvement I'd guess it's more from the anti-inflammatory effects of antibiotics.

I think the medical establishment has basically made this happen by ignoring these complex illnesses, so then people don't trust science at all and just flock to quacks on the opposite end of the spectrum--people that will just prescribe antibiotics for years with no evidence to back it up... it's too bad, all around people are being taken advantage of.

 

[Hip]

Then that patient with symptoms that match broad ME/CFS symptoms has a parvovirus. Why even bother with the ME/CFS label?

Well for one thing, because parvovirus B19 can cause several illnesses, so saying that you have a chronic parvovirus infection does not by itself specific which illness that infection has given you. The same is true of other pathogens.

 

[duncan]

But ME/CFS is almost certainly a complex metabolic/autoimmune response to pathogens/stressors/etc...

Metabolic markers are effects of some cause. They can be used like cytokine profiling is suggested to be used, at least in theory. Autoimmune response is one's own body inexplicably treating itself or part of itself like an antigen, at least, again, in theory. Both I suppose are thought by some to be triggered by infections/stressors, but not maintained, at least as far as ME/CFS is concerned.

That doesn't at all mean that there can't also be low-level viral infections, although I don't think the data on that is as robust as the data on metabolic/immune disturbances.

The key word in this observation is "also". If the low-level infection is the cause of the immune response, then the patient suffers from that low-level infection, definitionally. The problem here is that not many researchers - and certainly not many clinicians - think this is the case.

I am more looking forward to IVIG

As am I.

Lyme triggered my CFS but i'm not on antibiotics. i have found the chronic lyme community toxic in some ways.

I would advise looking outside the community and learning the history for yourself. You may come away surprised.

yes, there is some evidence that suggests borrelia can survive a standard course of antibiotics, but everywhere i look in the chronic lyme community, people are on years-long IV antibiotic courses with no way to measure whether the infection is gone or not (because they don't trust the standard tests, maybe for good reason) and they don't generally seem to be improving much. If there is improvement I'd guess it's more from the anti-inflammatory effects of antibiotics.

A lot to unpack here. I repeat my advice that you look into the history of the disease discovery in the US, and the evolution of the three key diagnostics, and the associated medical politics.

I think the medical establishment has basically made this happen by ignoring these complex illnesses

Agreed.

Well for one thing, because parvovirus B19 can cause several illnesses, so saying that you have a chronic parvovirus infection does not by itself specific which illness that infection has given you.

If you had a treatment for that parvovirus you should be able to mitigate most if not all of its downstream effects, except for those associated with tissue/organ damage. Same holds true for most other pathogens, I would imagine. By obscuring the cause of a cluster of symptoms with a contrived or misapplied syndrome or malady or infection, you make it more difficult to resolve the root disease.

 

[frozenborderline]

Metabolic markers are effects of some cause. They can be used like cytokine profiling is suggested to be used, at least in theory. Autoimmune response is one's own body inexplicably treating itself or part of itself like an antigen, at least, again, in theory. Both I suppose are thought by some to be triggered by infections/stressors, but not maintained, at least as far as ME/CFS is concerned.


The key word in this observation is "also". If the low-level infection is the cause of the immune response, then the patient suffers from that low-level infection, definitionally. The problem here is that not many researchers - and certainly not many clinicians - think this is the case.

I think this is really mistaken. This is probably the last post I'll make because neither of us are scientists I assume and most of this is speculation. WHile a low level infection could be the cause of an immune problem or metabolic problem, I don't think it makes sense that that has to be the case. Autoimmune diseases are one example of that not being true, but also naviaux's example of Dauer is relevant because it's a model of how an initial stressor can cause an extended metabolic alteration . Theoretically any stressor could do this, but a pathogen combined with either genetic abnormalities or environmental stress or already weak metabolism could initiate this issue.

I don't know why it would be impossible for an initial infection to cause a long term alteration in metabolism... these metabolic and purinergic systems are complex and don't have totally perfect regulating mechanisms, they can be thrown out of "homeostasis" (a word in quotes because i don't think it takes into account the complexity of regulation of different biological systems.

I'm totally open to the idea that viruses cause cfs. I just have looked at a lot of the evidence and don't think the theory that a chronic infection causes the symptoms is the most likely. I think naviaux's and ron davis' work so far is the strongest.

 

[msf]

Epstein-Barr virus is also well established as a trigger, as several studies have shown that around 1 in 10 patients who have mononucleosis will go on to get ME/CFS.





They would certainly be worth studying more, to see if they can shed light on the mechanisms of ME/CFS.


Dr Jonanthan Kerr had the idea of studying parvovirus ME/CFS to see if this could shed more light on the mechanisms of ME/CFS in general.

Parvovirus ME/CFS is quite unique, in that it is the only form of ME/CFS in which there is a classic and obvious chronic viral infection in the blood. Parvovirus ME/CFS is caused by a normal ongoing viral infection, with lots of viral particles to be found in the blood, which explains why you feel sick.

Whereas with enterovirus and herpesvirus ME/CFS, there is no classic chronic viral infection to be found in the blood (which is why blood PCR is often negative). The enterovirus and herpesvirus infections in ME/CFS are more mysterious. In the case of enterovirus ME/CFS, we know that this virus is hidden inside cells a chronic non-cytolytic intracellular infection.

That's why lots of people doubt the viral hypothesis of ME/CFS in the case of enterovirus and herpesvirus, because blood PCR will often be negative, so skeptics say: "where's the infection?"

But with parvovirus ME/CFS, nobody doubts that a viral infection causes it, because that infection is obvious to see.

Yes, good point about parvovirus. I think the Dubbo study showed long-lasting fatigue after mono, but I'm not sure how long the study was.

 

[duncan]

WHile a low level infection could be the cause of an immune problem or metabolic problem, I don't think it makes sense that that has to be the case. Autoimmune diseases are one example of that not being true, but also naviaux's example of Dauer is relevant because it's a model of how an initial stressor can cause an extended metabolic alteration . Theoretically any stressor could do this, but a pathogen combined with either genetic abnormalities or environmental stress or already weak metabolism could initiate this issue.

I do not disagree with this. I am saying that if an infection IS present, it may in fact be the culprit. Doctors should be pursuing this infection sometimes as the agent. But for many reasons, mostly due to crappy diagnostics, they do not. Use Lyme as an example. If NeuroLyme is behind neurological problems, it would be counterintuitive NOT to try to treat with ABX, or to ignore and throw LDN at it, yes? Extend that to other pathogens.

But I also subscribe to the idea that Lyme and enteroviuses and parvoviruses and EBV etc can induce (and then be resolved, so not be responsible for sustaining) immune dysfunction on a grand scale and even bring about a dauer state as suggested by Naviaux and company.

I am just saying, where an active infection can be determined to be at play, and could be responsible for the symptoms, it seems odd to pretend it isn't there and may not be the culprit. Where that disease IS responsible for the symptom cluster, then the patient has that disease as the cause, definitionally.

I am also suggesting I don't think many researchers are exhausting the search for pathogens when screening their ME/CFS cohorts. For example, how many are testing tissue samples, and by what constraints?

Sorry if I have been poor at my explanations. I really do applaud what Davis and Naviaux and others are doing.

 

[frozenborderline]

I do not disagree with this. I am saying that if an infection IS present, it may in fact be the culprit. Doctors should be pursuing this infection sometimes as the agent. But for many reasons, mostly due to crappy diagnostics, they do not. Use Lyme as an example. If NeuroLyme is behind neurological problems, it would be counterintuitive NOT to try to treat with ABX, or to ignore and though LDN at it, yes? Extend that to other pathogens.

But I also subscribe to the idea that Lyme and enteroviuses and parvoviruses and EBV etc can induce immune dysfunction on a grand scale and even bring about a dauer state as suggested by Naviaux and company.

I am just saying, where an active infection can be determined to be at play, and could be responsible for the symptoms, it seems odd to pretend it isn't there and may not be the culprit.

I am also suggesting I don't think many researchers are exhausting the search for pathogens when screening their ME/CFS cohorts. For example, how many are testing tissue samples, and by what constraints?

Sorry if I have been poor at my explanations. I really do applaud what Davis and Naviaux and others are doing.

It's certainly possible as an explanation and I hope that diagnostic technology improves a whole lot. I also hope that a lyme vaccine is invented.

Still I think that it's limited to only think of antiviral and antibiotic therapy. Hopefully in the future, our understanding of metabolism and holistic health improves so that we think of treating the metabolism and immune system so robustly that we can use antibiotics and antivirals less. They do have some harmful effects.

 

[Hip]

I think the Dubbo study showed long-lasting fatigue after mono, but I'm not sure how long the study was.

I have seen six different studies on fatigue or ME/CFS appearing after mononucleosis. This study is a good one; it found that at 6, 12 and 24 months after mononucleosis, 13%, 7% and 4% of the mono patients respectively met the criteria for ME/CFS.

 

[msf]

I have seen six different studies on fatigue or ME/CFS appearing after mononucleosis. This study is a good one; it found that at 6, 12 and 24 months after mononucleosis, 13%, 7% and 4% of the mono patients respectively met the criteria for ME/CFS.

Interesting - I thought that prospective Jason study that never seemed to materialise was supposed to test this hypothesis, but perhaps that was in relation to adult ME.

 

[msf]

Think you misread Duncan, or you are unaware that symptoms have been shown to track with cytokine levels.

 

[msf]

Ah, I hadnt refreshed my screen. I see you did misread him, debored.

 

[jesse's mom]

this is really giving me second thoughts re: my current use of antivirals

I bet!