High CMV IgG titers. What to do?

[alalush]

I have high IGG viral titers for CMV and EBV.
Especially CMV concerns me cause I have also a lot of heart complains (well they actually never found something, I had extensive research done: MRI heart, VO2max, ECG etc) But then my CMV was low probably. Do I need to take something for this high IgG ?

 

[MErmaid]

I have high IGG viral titers for CMV and EBV.
Especially CMV concerns me cause I have also a lot of heart complains (well they actually never found something, I had extensive research done: MRI heart, VO2max, ECG etc) But then my CMV was low probably. Do I need to take something for this high IgG ?View attachment 1254

I am not aware of anything you can take related to your high CMV and EBV test results that would help your heart. It sounds like you already had all of the right testing done, regarding how your heart functions. I assume you had an echocardiogram? I am not familiar with a heart MRI.

 

[jpcv]

Pretty good question, my CMV titers are high, like your s, altough my EBV titers are normal.
Dr Lerner did some heart biopsies in patients like us and found viral particles in the heart.
He studied the patients with 24 hrs Holter and scintilography before performing the biopsies and found T wave alterations in Holter and abnormal wall movment in the MUGA scans.
Have You done this tests?

 

[Jonathan Edwards]

Do I need to take something for this high IgG ?

You need to take advice from your physician. However, high antibody levels simply show a good level of antibody-based immunity to viruses. They do not in themselves indicate current infection or any need for treatment.

 

[Hip]

high antibody levels simply show a good level of antibody-based immunity to viruses. They do not in themselves indicate current infection or any need for treatment.

This has been the perennial debate in ME/CFS: what is the meaning of the high antibody titers usually found in ME/CFS?

Some believe that the high antibody titers found in ME/CFS patients are just the result of a dysfunctional immune system, and not the result of any ongoing infection, especially because PCR blood tests usually find no evidence of viruses in the blood.

But the other view is that these high titers are the result of an ongoing non-cytolytic infection (in the case of enteroviruses) or an abortive infection (in the case of herpesviruses).

In both non-cytolytic and abortive infections, you have an ongoing intracellular infection, but no new viral particles are produced. This is the characteristic of non-cytolytic and abortive infections; they do not produce any new viral particles, yet remain in the cells as chronic infections.

This may thus explain why there are high antibody titers in ME/CFS, yet when you perform PCR testing on the blood, you usually get a negative result, because there is no viremia. (But if you perform a PCR on the muscle tissues, you often find enterovirus RNA in cases of enterovirus-associated ME/CFS).




I have myself only recently really fully understood this business of high antibody titers in ME/CFS, but typically negative blood PCR results.

What made the penny drop for me was reading about Dr Martin Lerner's abortive herpesvirus infection theory of ME/CFS. After reading this theory (it is a theory — there is not much supportive evidence for it at present), it made me realize that enterovirus ME/CFS and herpesvirus ME/CFS may both be cases of chronic infections in the tissues which don't produce new viral particles.

 

[Jonathan Edwards]

This has been the perennial debate in ME/CFS: what is the meaning of the high antibody titers usually found in ME/CFS?

I don't think there is any serious debate here within the general research community. Dr Lerner came up with this strange theory years ago and when I looked at his explanation of the case he seemed to wander off into irrelevancies. Other than him I doubt you will find a virologist who takes this seriously. His theory is pure speculation without any empirical evidence. The alternative standard explanation for antibody titres - that they are a normal response to past infection - is perfectly reasonable and consistent with masses of evidence. There is absolutely no need to propose non-cytolytic infections. Antibody titres vary widely between normal people for reasons we understand pretty well. So I think it is important to get some sort of balance in the debate. Theories of smouldering infections have been chased time and time again by people like Lipkin and Hornig and Ron Davis and nothing found.

 

[Hip]

Other than him I doubt you will find a virologist who takes this seriously. His theory is pure speculation without any empirical evidence.

Yes, Lerner's theory does certainly lack empirical evidence, but the same cannot be said for enterovirus non-cytolytic infections, which can be thought of as a sort of abortive infection.

Without non-cytolytic infection, you cannot really explain what is going on in chronic coxsackievirus B myocarditis, in which you are almost never able to isolate and culture virus from the adult heart, yet the heart muscle contains enterovirus RNA. That cannot be explained by a regular enterovirus infection. It was through studying CVB myocarditis that non-cytolytic enteroviruses were discovered.

And the British enterovirus ME/CFS research found the same thing: ME/CFS patients muscles were often PCR positive for enterovirus RNA, but no virus could be isolated from the muscle biopsies. So again you cannot explain this by a regular enterovirus.

This 1991 paper says:

Attempts to demonstrate either infectious virus or virus-specific antigens in muscle samples 11 from PVFS patients had been consistently unsuccessful

Unfortunately in the 1980s and 90s, which were the hay-day of the British enterovirus ME/CFS research, nobody knew about non-cytolytic enteroviruses.


A blow to the enterovirus theory of ME/CFS arose from this 1994 paper, which found that patients with neuromuscular disorders also had enterovirus RNA in their muscles. So the authors concluded that it was unlikely that persistent enterovirus infection plays a pathogenetic role in ME/CFS. However, this conclusion does not seem to take into account the possibility that enterovirus infections elsewhere (such as the brain) may also be involved in ME/CFS.

 

[Jonathan Edwards]

It is always possible that there are peculiar modes of infection used by very unusual viruses but in general none of this impacts a general approach to antibody titres. Chasing wisps of straw in the wind when you have a bale sitting beside you seems to me unproductive.

 

[Hip]

It is always possible that there are peculiar modes of infection used by very unusual viruses but in general none of this impacts a general approach to antibody titres. Chasing wisps of straw in the wind when you have a bale sitting beside you seems to me unproductive.

Just for reference purposes, here is Dr Chia's slide of enterovirus antibody titers in 200 ME/CFS patients versus 150 healthy controls:

Enterovirus antibody titers of ME/CFS patients versus healthy controls

Source: Dr John Chia, Invest in ME London Conference 2009​

The healthy controls were typically healthy spouses or relatives of the patients who came into Dr Chia's clinic with the ME/CFS patient.

So although lots of ME/CFS patients have antibody titers no different to those of healthy controls, there is an overall trend for ME/CFS patients to have higher titers than the controls.


And similarly in a 1984 UK study, 38% of 81 ME/CFS patients at a Scottish general practice had Coxsackie B titers over 1:256 (and these were not rising titers), whereas when 1,000 adults of the general population were tested, only 10% had titers over 1:256.

 

[alalush]

Maybe I need to take Gammanorm again. Since my total IGG is on the low side, will measure again subclasses. Last time IGG4 was slightly too low.