Giancarlo Sal y Rosas
Herpes Simplex Virus type 2 (HSV-2) is the main caused of Genital Herpes, although HSV-1 accounts for about half of new cases in developed country. HSV-2 infection is endemic and transmission most frequently occurs by contact with a person who is shedding virus at a peripheral area, mucosa surface, in genital or oral secretions. The biological cycle of HSV-2 infection covers initial infection, latency, reactivation and transmission.
HSV-2 primary infection or symptomatic reactivation induce two potential biological bridges for HIV acquisition: (a) a break in the genital mucosa will bring HIV free cells virus in direct contact with its susceptible targets such as activated CD4 T cells and macrophages that live in the sub epithelium. (b) The presence of HSV-2 virus induces a response of the immune system and therefore an increase in the number of HIV susceptible target cells.
Moreover, in the last few years, scientists have discovered that most of HSV-2 reactivations are short and asymptomatic. In a group of HSV-1 (n=18 ) and HSV-2 positive patients (n=25), the median number of reactivations was 1.5 per moth and 50% of anogenital last less than 12 hours and only 7% of those were symptomatic. We will discuss how the immune system reacts under asymptomatic reactivations and the hypothesis that even asymptomatic reactivations potentially increase HIV acquisition.
To understand the association between HIV-1 and HSV-2, we will discuss, in the first part of my presentation, a little bit of HIV virion, the mechanics of HIV acquisition and what the principal HIV target cells are. The second part of my biology project will discuss HSV-2 infection, in particular primary infection and how the immune system responds to the infection. We will also discuss latency and reactivation (frequency of reactivations) of the virus. Finally, we will discuss potential mechanics that could increase HIV susceptibility in HSV-2 positive patients. Moreover, we will discuss the results of a double blind, randomized; phase 3 clinical trial that tested whether using acyclovir to suppressed HSV-2 in HSV-2 positive patients can reduce HIV acquisition.
