@rodgergrummidge, what I am saying is that chronic high titers are often found in ME/CFS patients, but nobody knows what these high titers signify. If you believe that the high titers simply reflect a past infection, that's a valid interpretation, but it is only an interpretation, not a fact as such. However, an equally valid interpretation is that there is an ongoing infection in the tissues of ME/CFS patients that causes the high titers. This is usually how the ME/CFS specialist doctors interpret the high titers. Here are Dr John Chia's validation tests for enterovirus antibody titers of 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. As you can see, 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. Several of the British research papers on enterovirus-associated ME/CFS found similar raised titers in ME/CFS. I agree that if an ME/CFS doctor finds high titers in his patients, this is not diagnostic of ME/CFS; but given Dr Chia's data above, high titers do help support the ME/CFS diagnosis. More to the point, high titers help indicate which antivirals/immunomodulators would be appropriate for the patient. If a patient has high enterovirus titers, then you would want a treatment that fights enterovirus. Whereas if the patient has high herpesvirus titers, then a herpesvirus antiviral will be needed. I believe that's the main reason ME/CFS doctors test for viruses; it's more to help select the right antiviral treatment, rather than for diagnostic purposes. But what evidence is there for ongoing infection in the tissues of ME/CFS patients? As I mentioned, in the case of enterovirus-associated ME/CFS, there is plenty of evidence of ongoing infection. If you look at this post listing the early British ME/CFS enterovirus research, and do a find on the word "muscle," you will pick up all the studies in that post that found enterovirus RNA in the ME/CFS patients muscles. In spite of there being enterovirus RNA in the muscles in ME/CFS, no virus could be cultured from the patients' muscle samples. Thus this shows the muscle infection in ME/CFS is not an ordinary productive infection, as it does not produce viral particles. We now know that this muscle infection is a non-cytolytic enterovirus infection, which is an abortive infection of sorts (non-cytolytic enterovirus infections are ongoing, but produce no new viral particles). Enterovirus researchers think that this non-cytolytic infection may be the cause of ME/CFS in the enterovirus subset. I started this thread to explain a bit about the non-cytolytic enterovirus. As regards evidence for abortive EBV, HHV-6 and cytomegalovirus infections in ME/CFS, there is very little at this stage. But I think you will agree that for enterovirus, there is good evidence. I believe in the case of coxsackievirus B dilated cardiomyopathy, which involves non-cytolytic infection of the heart muscle, high titers to CVB are often found. So this suggests that non-cytolytic infection can lead to high titers.