By Jill McLaughlin
Human Herpesvirus 6 (HHV-6) is one of eight known members of the human herpesvirus family. The virus, which was discovered in 1986 at the NCI, infects cells of the immune and central nervous system.
Serologic testing demonstrates that more than 95% of the worlds population is positive for antibodies to HHV-6, indication an immune response to infection by the virus. After initial infection, HHV-6 viral DNA remains latent within the cell nuclei in blood and other body tissue.
Two variants of HHV-6 are recognized: HHV-6A and HHV-6B. Primary infection with HHV-6B causes roseola in children and more than 95% of the population has antibodies to this variant. Primary infection with HHV-6A is believed to occur late childhood or adulthood and may occur without symptoms. The A strain is much more pathogenic and attacks the brain and immune system. The prevalence of HHV-6A infection is not known.
HHV6-A reactivation in adulthood can result in illness. Normally, reactivations are kept in check by the immune system and the virus resumes latency. Reactivation in adults has been associated with mononucleosis syndrome, autoimmune disorders, and nervous system diseases. HHV-6 has been specifically linked to MS, AIDS and CFS.
In individuals whose immune system has been compromised by disease (AIDS) or medical treatments (chemotherapy or immunosupressive drugs), a reactivation of HHV-6 can result in suppression of bone marrow function or inflammation and cause damage in tissues such as brain, liver, or lungs.
Recent studies have revealed active HHV-6 infections in single random blood samples taken from MS patients (54% positive) and CFS patients (39% positive). After testing a second sample from patients who were negative, 24% tested positive for active infection. Results showed that on average these samples were positive 50% of the time. This suggests that active infection of HHV-6 may be intermittent, with the viral load changing over time.
Normal healthy controls were negative for active HHV-6. This demonstrates that active HHV-6 infections are abnormal and not found in healthy people without disease associations.
Dr. Ablashi found that 70% of the HHV-6 isolates from patients were variant A, which is more neurotropic. He found that CFS patients exhibited HHV-6 DNA in the cerebrospinal fluid (CSF) and was able to infect cord blood cells with CSF from these patients. He concluded that HHV-6 may well account for the neurological manifestations in CFS patients.
In addition there is a wide spectrum of lymphoid, hematopoetic and autoimmune diseases which are associated with elevated titers of HHV-6, from which replicating virus has been isolated. Such diseases include atypical polyclonal lymphoproliferation, Hodgkin’s disease, CFS and systemic lupus erythematosis.
Contrary to the findings of the CDC, HHV-6 can account for many of the clinical symptoms of CFS. The problem with the CDC testing, says Knox and Cartrigan, is that “it tested both patient and control groups using serum samples, lymphocytes and three PCR methods.” These are not adequate means of detecting active HHV-6 infection.
The ability of HHV-6 to induce high level production of proinflammatory cytokines, combined with its frequent infection of the brain and spinal cord and its ability to infect and destroy all types of lymphocytes (including NK cells whose function is known to be impaired in CFS patients) can account for a range of clinical abnormalities that define CFS.
Whether or not these agents are causative, many studies have suggested that persistent viral activity plays a role in the perpetuation of symptoms. The good news is that the possibility exists that CFS may be effectively treated with currently available anti-viral medications. Longitudinal studies of antivirals are required to determine precisely what role HHV-6 infection plays in the pathogenesis of the disease.
An association for CFS
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