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Does Infection or Reactivation of HHV-6 Play a Role in the Development of Multiple Sclerosis (MS) and Chronic Fatigue Syndrome (CFS)?

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By Ablashi DV, Eastman HB, Owen CB, Roman MM, Friedman J, Zabriskie JB, Peterson DL, Pearson GR, Whitman JE • www.ProHealth.com • May 4, 2000


Summary
Human Herpes Virus-6 (HHV-6) is a universal virus. Infection usually occurs during childhood, after which it generally turns dormant within the body. Presently, the reactivation of HHV-6 has been shown to play a role in the development of AIDS and several other diseases.

Armed with this information, doctors at Georgetown University's School of Medicine conducted a clinical study to determine what role HHV-6 infection or reactivation plays in the development of MS and CFS.

HHV-6 IgG and IgM antibody levels were measured in 21 MS and 35 CFS patients. Peripheral blood mononuclear cells (PBMCs) were also analyzed for the presence of HHV-6. These same levels were measured in a healthy control group. Compared to the control group's levels, both MS and CFS patients had significantly increased levels of HHV-6 antibody and HHV-6 DNA. A decrease in cellular immune responses was also detected in CFS patients. This new data suggests that the reactivation of HHV-6 may play a role in the development of MS and CFS.



Abstract
Ablashi DV, Eastman HB, Owen CB, Roman MM, Friedman J, Zabriskie JB, Peterson DL, Pearson GR, Whitman JE

Department of Microbiology and Immunology, Georgetown University, School of Medicine, Washington, DC, USA.

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.

Source:
J Clin Virol 2000 May;16(3):179-91 PMID: 10738137, UI: 20204458




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