quick snap shot of the article.
Herpesviruses -- One of the more intriguing connections involves herpesviruses. Herpesviruses infect B-cells and replicate in great numbers during B cell transformation. Killing B-cells before they get transformed or activated could reduce or even cause a herpesvirus infection to die out as the B-cells they have infected die over time.
Rituximab has been studied in EBV related diseases and two studies underway appear to be focusing on its effects on herpesviruses.
The NIAID awarded Marcia Blackman at the Trudeau Institute $235,000 to examine B-cell depleting antibodies and herpesviruses in mice with an eye towards stopping the development of B-cell lymphomas in transplant patients. The broad research community has yet to embrace the importance of herpesviruses in ME/CFS but there is no doubt as to their virulence in other areas. The immunosuppression organ transplant patients require increases their risk of EBV associated B-cell lymphoma.
Dr. Blackmans goal is to determine whether a b-cell depleting antibody can lower the latent load or even to purge latency from the host; ie to completely cleanse the mices system of herpesvirus infected cells. Dr. Ann Arvin at Stanford also has a grant to study Protective Immunity against herpesviruses that may appears to involve Rituximab as well.
http://projectreporter.nih.gov/proje...0&icde=5938112
XMRV? - the recent announcement from Spain that XMRV has been found in B-cells suggests that, if that finding is validated, Rituximab's effectiveness in some people could be due to reducing XMRV loads. If XMRV works out this could, in fact, be a more viable explanation than herpesviruses because the positive XMRV study results suggest XMRV may be more prevalent in the ME/CFS population than herpesviruses.
