It is well established that many pathogens may cause sexually transmitted diseases (STD). In this study, a monoclonal antibody was produced against HHV-6B REP (anti-REP mAb). Like adeno-associated virus type 2 Rep68/78, HHV-6A ts suppressed H-ras transformation of NIH 3T3 cells. We found that replication of HSV-2 in HeLa cells and in 86HG39 cells is inhibited after stimulation of the cells by IFN-γ and TNF-α. The HSV gene RL1 (γ134.5; neurovirulence factor) is not present in HVP-2, as is the case for SA8 and B virus. Finally, randomised controlled trials have been conducted in coinfected individuals to evaluate the effect of HSV-2 suppressive therapy on HIV-1 genital shedding and plasma HIV-1 RNA, showing, in most cases, a negative impact on HIV-1 replication [5–7]. Moreover, UL56 relocalized Nedd4 to the vesicles in cells transiently expressing UL56 and in cells infected with HSV-2.
1. Purchase, H. A 2-year-old male marmoset (Callithrix jacchus) was brought to a veterinary clinic with a 6-day history of severe necrotizing stomatitis, vomiting, and loss of appetite. ts suppressed expression from both wild-type and upstream mutant HIV-1 LTR-CAT constructs. However, downstream HIV-1 TAR mutations reversed ts suppression, indicating that TAR is one of the critical elements involved. The data presented demonstrated that HHV-6A ts functionally suppressed H-ras transformation and HIV-1 LTR expression and thus that it may be useful in future gene therapy.