Study "No serological evidence for a role of HHV-6 infection in chronic fatigue syndrome"

A negative HHV-6 study from Bethesda.

No serological evidence for a role of HHV-6 infection in chronic fatigue syndrome

Peter D Burbelo, Ahmad Bayat, Jason Wagner, Thomas B Nutman, James N Baraniuk, Michael J Iadarola

National Institutes of Health, Bethesda, MD
Georgetown University, Washington, D.C.

Abstract:
Human herpesvirus 6A (HHV-6A) and human herpesvirus 6B (HHV-6B) are associated with a variety of conditions including rash, fever, and encephalitis and may play a role in several neurological diseases.

Here luciferase immunoprecipitation systems (LIPS) was used to develop HHV-6 serologic diagnostic tests using antigens encoded by the U11 gene from HHV-6A (p100) and HHV-6B (p101).

Analysis of the antibody responses against Renilla luciferase fusions with different HHV-6B p101 fragments identified an antigenic fragment (amino acids 389 to 858) that demonstrated ~86% seropositivity in serum samples from healthy US blood donors.

Additional experiments detected a HHV-6A antigenic fragment (amino acids 751-870) that showed ~48% antibody seropositivity in samples from Mali, Africa, a known HHV-6A endemic region.

In contrast to the high levels of HHV-6A immunoreactivity seen in the African samples, testing of US blood donors with the HHV-6A p100 antigenic fragment revealed little immunoreactivity.

To potentially explore the role of HHV-6 infection in human disease, a blinded cohort of controls (n=59) and chronic fatigue syndrome (CFS) patients (n=72) from the US was examined for serum antibodies.

While only a few of the controls and CFS patients showed high level immunoreactivity with HHV-6A, a majority of both the controls and CFS patients showed significant immunoreactivity with HHV-6B.

However, no statistically significant differences in antibody levels or frequency of HHV-6A or HHV-6B infection were detected between the controls and CFS patients.

These findings highlight the utility of LIPS for exploring the seroepidemiology of HHV-6A and HHV-6B infection, but suggest that these viruses are unlikely to play a role in the pathogenesis of CFS.

Not really a particularly large CFS patient cohort in this study. Especially considering that I don't know how the CFS patients were selected, nor by whom – none of the names ring a bell for me.

While I don't think that any one of the herpes viruses is the root cause of ME/CFS, this study from Bethesda does not instill confidence for me – oh well.

Here we have researcher from Bethesda who know something about HHV-6, but I don't know if they know much about CFS patient populations. And then here we researchers from Latvia who don't seem to know much about HHV-6, but may (or may not) know more about CFS. And those who know both HHV-6 and CFS produce underwhelming results. It's a sad world.