An anti-HIV drug also discovered to stop the spread of the genital herpes virus does so by disabling a key DNA enzyme of the herpes virus, according to findings by researchers at the National Institutes of Health and other institutions. A Poisson multivariable model was used to estimate adjusted incidence rate ratios of HIV acquisition associated with HSV-2 and other covariates. Shingles is probably the most painful thing I have ever encountered. This stimulation was seen at both their permissive (34 degrees C) and nonpermissive (39 degrees C) temperatures, implying either that HSV-1 infection or immediate-early gene expression is all that is required. RESULTS: HIV-1 RNA was detected from lesional swabs in 25 of 26 consecutively studied HSV-2 episodes and on 67% of days in which genital lesions were noted. Plausibly, antiherpetic therapy could reduce HIV transmission by decreasing HIV plasma load and/or mucosal HIV shedding, but a proof-of-concept trial is needed to demonstrate this. Research involving people who have not taken HIV treatment (who are antiretroviral naive) has also shown that some human herpes viruses including CMV and EBV can cause immune activation or increase viral load in semen.
“Once these cells are activated and busy trying to find the herpes, their activation means that they are in the exact state they need to be in for HIV to infect them,” explained Johnston.