Nov 15, 2007
pls doc i am hiv poz and i have got a cold sore on my lip,will this effect my viral load and cd4?i did have herpes genital last year on my anus and my penis,scared of it all coming back pls answer as my doctors always hard to track and have to make appointment 1 week later i would like to now now if possible thanx
Response from Dr. Frascino
Actually any active infection, including herpes, can transiently affect plasma HIV viral load and CD4 counts. You may want to wait until your current outbreak subsides to have your blood drawn for routine follow-up studies. Also, since you are HIV positive and have had multiple outbreaks of herpes genital and now lip you might want to consider suppressive therapy with an anti-herpes drug. There have been some recent studies suggesting herpes suppression may improve long-term survival in HIVers. (See below.)
Finally, what's this nonsense about your doctor's being hard to track??? If your HIV specialist isn't responsive to your needs or available when you need him or her, it's time to find a new, more reasonable, HIV specialist!
Anti-herpes treatment reduces HIV levels; treatment or vaccine urged for HIV prevention
Keith Alcorn, Wednesday, February 21, 2007 Control of herpes simplex with daily treatment or with a vaccine should be considered as a strategy to reduce HIV transmission, urge researchers who carried out a large randomised study of the effects of an anti-herpes drug on HIV in African women. Their findings are published in the February 22nd edition of the New England Journal of Medicine.
The ANRS 1285a study, funded by the French Agence Nationale de Recherches sur le Sida (ANRS) and the United Kingdom's Department for International Development, was first presented at the 2006 Conference on Retroviruses and Opportunistic Infections in Denver (click here for full results).
The study showed that HIV-positive women randomised to receive daily treatment with valaciclovir, an anti-HSV2 drug, had lower amounts of HIV in their genital fluids and in their blood. These women were not receiving antiretroviral treatment.
The reduction in plasma viral load at the end of the three month study was 0.5 log10, a decline associated with a reduction in the risk of disease progression, notes Dr Lawrence Corey of the University of Washington, Seattle, in an editorial accompanying the study report.
The authors point out that the degree of viral load suppression increased with time on treatment, suggesting that a longer duration of treatment with valaciclovir might lead to a greater reduction in viral load. Longer studies are needed, they say, to examine the impact both on HIV disease and HIV transmission.
Valaciclovir appears to exert its effect on HIV viremia not through direct mechanisms, but by reducing HSV-2 levels. The authors speculate that reducing HSV-2 levels may reduce the activation of cells latently infected with HIV (HSV-2 can activate latent HIV), and discourages clinical episodes of herpes simplex that lead to an upsurge of HIV replication. Replication of HSV-2 without symptoms may have the same effect.
Dr Philippe Mayaud, one of the researchers from the London School of Hygiene and Tropical Medicine who carried out the study, said: "Our results have important potential implications for public health and clinical practice, as HSV-2 control could become a new form of HIV prevention targeting HIV-infected individuals, as well as providing clinical benefits."
"Importantly, an HSV vaccine that would either prevent HSV infection or diminish the clinical and sub-clinical manifestations of HSV with a similar efficacy on HIV as HSV suppressive therapy, would represent a long-lasting form of HIV prevention. The development and evaluation of an HSV vaccine should rank high on the international research agenda."
Nagot N et al. Reduction of HIV-1 RNA levels with therapy to suppress herpes simplex virus. N Engl J Med 356 (8): 790-99, 2007.
Corey L. Synergistic copathogens HIV-1 and HSV-2. N Engl J Med 356 (8): 854-856, 2007.
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