SUMMARY: It is not unusual to carry the virus HHV-6. Most people become infected with it as children, but just never develop an active infection. But what happens when HHV-6 does develop into infection? Researchers understand that when “reactivated” HHV-6 encourages the rise of certain diseases, including AIDS. This study proposes that another one of the diseases for which HHV-6 bears responsibility is chronic fatigue syndrome (CFS). To this end, researchers took various measurements of HHV-6 in 35 patients with CFS. Compared to the patients in the control group, their levels of HHV-6 were found to be quite high. Measuring different forms of HHV-6 yielded percentages of 54% and 57% for CFS patients, compared to just 8% and 16% for the healthy patients.
They also found that in the course of two and a half years, two of their CFS patients were plagued by persistent HHV-6 infection. Plus, ten of the CFS patients registered cellular immune responses that centered on HHV-6. The increased levels of HHV-6 antibody and HHV-6 DNA in CFS patients, coupled with their decreased cellular immune responses, support the hypothesis that reactivating HHV-6 plays some part in the genesis of CFS.
ABSTRACT: Background: HHV-6 is a ubiquitous virus and its infection usually occurs in childhood and then becomes a latent infection. HHV-6 reactivation has been shown to play a role in the pathogenesis of AIDS and several other diseases. Objectives: To determine what role HHV-6 infection or reactivation plays in the pathogenesis of multiple sclerosis (MS) and chronic fatigue syndrome (CFS). Results: Twenty-one MS and 35 CFS patients were studied and followed clinically. In these patients, we measured HHV-6 IgG and IgM antibody levels and also analyzed their peripheral blood mononuclear cells (PBMCs) for the presence of HHV-6, using a short term culture assay. In both MS and CFS patients, we found higher levels of HHV-6 IgM antibody and elevated levels of IgG antibody when compared to healthy controls. Seventy percent of the MS patients studied contained IgM antibodies for HHV-6 late antigens (capsid), while only 15% of the healthy donors (HD) and 20% of the patients with other neurological disorders (OND) had HHV-6 IgM antibodies. Higher frequency of IgM antibody was also detected in CFS patients (57.1%) compared to HD (16%). Moreover, 54% of CFS patients exhibited antibody to HHV-6 early protein (p41/38) compared to only 8.0% of the HD. Elevated IgG antibody titers were detected in both the MS and the CFS patients. PBMCs from MS, CFS and HD were analyzed in a short term culture assay in order to detect HHV-6 antigen expressing cells and to characterize the viral isolates obtained as either Variant A or B. Fifty-four percent of MS patients contained HHV-6 early and late antigen producing cells and 87% of HHV-6 isolates were Variant B. Isolates from CFS, patients were predominately Variant A (70%) and isolates from HD were predominately Variant B (67%). Moreover, one isolate from OND was also Variant B. Persistent HHV-6 infection was found in two CFS patients over a period of 2.5 years and HHV-6 specific cellular immune responses were detected in PBMCs from ten CFS patients. Conclusions: In both MS and CFS patients, we found increased levels of HHV-6 antibody and HHV-6 DNA. A decrease in cellular immune responses was also detected in CFS patients. These data suggest that HHV-6 reactivation plays a role in the pathogenesis of these disorders.
“Frequent HHV-6 reactivation in multiple sclerosis (MS) and chronic fatigue syndrome (CFS) patients,” J Clin Virol 2000 May 1;16(3):179-191