CFS patients often show evidence of immune dysfunction and/or dysregulation, such as low suppressor cell numbers, low numbers and efficacy of NK cells, and abnormal RNase L. These dysfunctions are manifest when the immune system is challenged by a virus or other infection, suggesting that there might be a viral trigger that initiates and/or perpetuates CFS. Active infection by HHV-6 is found in association with patients suffering from CFS in significantly greater proportion than in the healthy immunocompetent population. In this "subgroup" of CFS patients, HHV-6 might be the viral trigger for CFS. The fact that HHV6 is not found universally in CFS patients might be because (a) other viruses/agents or events can also precipitate CFS by triggering faulty immune response; or (b) the nature of HHV-6, as with all herpesviruses, is cyclical and thus a "snapshot" of a group of CFS patients would also include those patients in the latent phase of chronic, recurring HHV-6 infection. Anecdotal evidence from some CFS patients we have observed, in some cases over many years, does reveal chronic, recurring HHV-6 reactivation. It must be noted that it is not clear whether HHV-6 actually plays a causative role in the development of CFS or is simply released from suppression when CFS occurs. There are at least three hypotheses that could explain the presence of active HHV-6 infection in a subset of CFS patients:
Hypothesis 1: HHV-6 is a primary co-factor (along with genetic, environmental, and/or co-infection conditions) in the development of CFS in a subset of patients.
Hypothesis 2: HHV-6 has no direct causative role in CFS, but exacerbates existing symptoms and further affects immune function; i.e. an indirect or supporting role in the condition of CFS.
Hypothesis 3: HHV-6 has no role in CFS, but is often found co-existing with CFS due to suppressed immune function in these patients; i.e. HHV-6 exploits a CFS-depressed immune system, but is otherwise unrelated to the symptoms of CFS.
Another HHV-6-related subgroup of CFS is that in which patients display CNS symptoms, including neurocognitive difficulties, such as memory impairment, "mental fog,'' and diminished concentration. These patients can display evidence of active HHV-6 infection in the spinal fluid. A higher proportion of HHV-6 in the spinal fluid appears to be of the A variant (compared with blood), suggesting that variant A is more neurotropic than variant B. It should also be noted that peripheral results for HHV-6 might not correlate with the HHV-6 status of the CNS (Hall et al., 1998). In CFS patients with HHV-6 in the spinal fluid, it is postulated that HHV-6 has a direct role in the illness, and the therapy to reduce the HHV-6 infection could be an effective treatment.
Treatment of CFS with antivirals (e.g. acyclovir, ganciclovir, foscarnet, cid-ofovir) or immunomodulating therapy (e.g. Poly I: Poly C12U, and IV gammaglobulin) has met with mixed success, further suggesting the need to identify CFS subgroups for whom specific effective treatment can be targeted.
Currently, all CFS patients are combined under this one diagnostic umbrella. Not surprisingly, universal causes and treatments have not been found, often leading to the conclusion that any one theory of cause or treatment is invalid. Here, two possible subgroups of HHV-6-related CFS are proposed: chronic, recurring HHV-6 reactivation in the periphery that precipitates or exacerbates CFS symptoms; and acute or chronic HHV-6 infection in the CNS.
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