Transmission of HIV to the placenta, fetus and mother and implications of gametic infection.

Therapeutic interventions and public education are reducing pediatric AIDS cases in developed countries, but the number of HIV-infected women and children is still a major global concern. The finding that human sperm-associated HIV can be transmitted to oocytes following in vitro fertilization provides a novel viewpoint from which to consider not only the problem of HIV transmission to children but also transmission to women. In the present paper we will first discuss some recent findings that offer new perspectives on the role of the placenta, and particularly the trophoblast, in maternal-fetal transmission of HIV.

Kinetics of HIV infection of human placental syncytiotrophoblast cultures: an ultrastructural and immunocytochemical study.

We previously demonstrated that syncytiotrophoblast (ST) cells from term human placentas could be infected when cocultured with HIV-infected lymphocytic cells. Here, we have used fluorescence microscopy and transmission electron microscopy to examine the kinetics of this infection process. Molt-4 clone 8 cells infected with HIV-1Lai or filtered supernatant from these cultures were incubated with ST cells for different times.

Simian immunodeficiency virus infection via amniotic fluid: a model to study fetal immunopathogenesis and prophylaxis.

The rising prevalence of infection with the human immunodeficiency virus type 1 (HIV-1) in young women will increase the number of infected children worldwide. Because HIV-1 seems to be transmitted mostly intrapartum, fetal infection probably occurs mainly via skin or mucous membrane exposure. A model for this route of fetal infection has been established in primates.

Pentoxifylline (Trental) decreases the replication of the human immunodeficiency virus type 1 in human peripheral blood mononuclear cells and in cultured T cells.

Pentoxifylline (Trental), used routinely for the treatment of intermittent claudication, has been shown previously to decrease the levels of tumor necrosis factors-alpha (TNF-alpha) RNA in cancer patients and to lead to a general improvement of well being. Increased TNF-alpha levels have been observed not only in cancer patients but also in cachectic patients with the acquired immunodeficiency syndrome (AIDS), and TNF-alpha is known to increase the expression of the human immunodeficiency virus type 1 (HIV-1) via activating its long terminal repeat (LTR). Moreover, TNF-alpha decreases the therapeutic efficacy of zidovudine (AZT).