The presence of concurrent sexually transmitted infections is an important co-factor in both sexual and mother-to-child transmission of HIV. Infections such as syphilis and herpes simplex virus type 2 (HSV-2) have been linked to increased risk of sexual transmission in gay men and in heterosexual men and women ^{[1] [2] [3]}, as well as to mother-to-child transmission in both industrialised and developing countries ^[4] [5].

Sexually transmitted infections can enhance sexual transmission by increasing HIV shedding in genital fluids. In addition, immune cells susceptible to HIV collect in areas of genital inflammation, and genital sores provide a route for viral entry.

Studies have shown that men with inflammation of the urethra (especially due to gonorrhoea or chlamydia) have a higher HIV viral load in their semen than men without urethritis, despite a similar blood viral load. Further, treating these infections with antibiotics reduces semen viral load^[6][7].

Syphilis infection in HIV-positive men has been linked to higher a HIV viral load in the blood and lower CD4 cell counts^[8]. A recent Spanish study found that although CD4 counts rose after syphilis was treated, viral load did not fall to the level seen in patients who never had syphilis^[9].

Active HSV-2 infection is associated with higher HIV viral load in blood and genital secretions in women^[10][11]. Some studies have also found an association between HSV-2 infection and elevated HIV levels in the blood, semen and rectal secretions in men.

Treating HSV-2 can reduce HIV viral load in the blood and genital fluids. A study in Burkino Faso, for example, found that daily valaciclovir (Valtrex) reduced genital shedding of HIV in both antiretroviral-treated and untreated women, whilst HIV in the blood also decreased in the women not taking anti-HIV therapy^[12]. A related but less expensive drug, aciclovir, produced more modest effects in studies in South Africa and Thailand^[13] [14].