View from HHV-6 and Virus Meetings

By Suzanne Vernon, PhD

Suzanne Vernon, PhD, is the Association’s scientific director. She has nearly two decades of experience as a microbiologist.

I recently attended the International Symposium on Viruses in Chronic Fatigue Syndrome and Postviral Fatigue, held in Baltimore, Maryland. This was a satellite meeting immediately following the 6th International Conference on HHV-6 and 7—organized by the HHV-6 Foundation and cosponsored by a number of organizations including the CFIDS Association.

The day-and-a-half symposium was packed with talks on viruses associated with or thought to trigger CFS, including HHV-6 and HHV-7, Epstein-Barr virus (EBV), parvovirus B-19, enteroviruses and borna disease virus. There were presentations on postinfectious fatigue, the host immune response and genomics in CFS. In addition, Jose Montoya, MD, presented the much- anticipated preliminary results of the randomized, double-blind, placebo-controlled trial of valganciclovir (also known as Valcyte) in CFS patients.

The take-home message from the symposium was not a new one: CFS is a heterogeneous mix of several subtypes, some of which may be triggered by infectious agents. Some of these infectious agents, particularly viruses, can stay with us for life and occasionally get reactivated. Antiviral drugs may be effective against some of these viruses. This is why the results of the valganciclovir treatment trial have generated great interest.

Valganciclovir is an antiviral drug used to treat cytomegalovirus infections by slowing virus growth. Cytomegalovirus, EBV, HHV-6 and HHV-7 are all herpes viruses, and valganciclovir has some effects on EBV, HHV-6 and HHV-7. The treatment trial conducted by Montoya included CFS patients who had elevated antibodies to HHV-6 and EBV, indicating that these viruses were reactivated. In the trial, 20 patients received valganciclovir and 10 patients received a placebo for a number of months. Patients receiving the antiviral drug reported improved cognitive and physical functioning over those receiving placebo.

It’s worth noting that the analyses of this drug trial are preliminary, and the study is small. Most physicians in the audience admitted they would not feel comfortable changing their approach to treating CFS until response markers and adverse events are determined through further analysis. Still, there is reason to be optimistic that valganciclovir may be effective for a specific subset of people with CFS—particularly those with elevated EBV and HHV-6 titers.

However, valganciclovir is not for everyone with CFS, and many questions regarding this drug need to be answered. For example, viruses quickly become resistant to antiviral drugs used to combat them, and cytomegalovirus is known to become resistant to valganciclovir. In addition, viruses like EBV and HHV-6 live in our cells, so when antiviral drugs target  these viruses, they can also affect proteins and processes essential for the health of our cells. In short, valganciclovir is a powerful drug that’s not without risk, and some the drug’s effects can be life-threatening.

I commend Montoya and his Stanford team for forging ahead with what could be a reasonable treatment for some CFS patients. But many questions must be answered before valganciclovir can be considered an effective treatment for CFS.

Look for more information on CFS and viral agents in the fall issue of the CFIDS Chronicle. If you don’t already subscribe to the CFIDS Chronicle, click here to join.

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