Herpesviruses, such as Epstein–Barr virus (EBV) or human cytomegalovirus (HCMV), were once thought to have a central role in ME/CFS, but this view now has little support. Why? Because there is not much evidence that people with the illness have high levels of viral DNA, herpesvirus antigens or immunoglobulin antibodies to herpesvirus.
Despite this, a research group in the USA has reported successful outcomes with long-term antiviral treatment for EBV or HCMV. These researchers reviewed the records of 142 ME/CFS patients, each of whom originally had raised levels of antibodies to herpesvirus, and who had completed six or more months of herpesvirus subset-directed antiviral therapy. In those who had no other tick-borne infections to complicate the clinical picture, 75% improved with therapy.
But the surprise was that improvements began to be seen at least six weeks into treatment — a fascinating observation causing the researchers to propose a paradigm to explain their findings (Virus Adaptation and Treatment, 2011). They speculate that herpesviruses do indeed infect ME/CFS patients, but that the initial infection is contained inside host cells where a variety of cellular disruptions occur, leading ultimately to symptoms but not the production of infectious new viral particles. This idea is consistent with the death of host cells seen in ME/CFS, and with the suggested effectiveness of antiviral therapies which interrupt the process, though only after a time-lag.
So, should all ME/CFS patients be given antivirals? Well, it is important to note that patients in this study had documented evidence of herpesvirus infection and had been prescribed antivirals for symptoms of infection; whether most ME/CFS patients in the population experience “non-permissive” herpesvirus replication remains to be proven. Furthermore, antiviral drugs are not without side effects, which can include neurotoxicity and reductions in red and white blood cells. So, medical advice is essential.
Reference: A paradigm linking herpesvirus immediate-early gene expression apoptosis and myalgic encephalomyelitis chronic fatigue syndrome. Lerner & Beqaj. Virus Adaptation and Treatment 2011: 3: 19–24.
