BACKGROUND Viruses cross the placenta and infect the fetus. Antivirals are administered to pregnant women to protect them and the fetus against the viruses. It is necessary to know which antivirals cross the placenta and reach the fetal circulation in pharmacologically significant concentrations in order to plan antiviral therapy. OBJECTIVE This article reviews the literature on the placental transfer of antivirals against HIV. The review considers also the placental transfer of acyclovir and ganciclovir, which are used against the herpes simplex virus and the cytomegalovirus, respectively. METHODS Firstly, a medline was performed with the following key words "placental transfer of antivirals". Secondly, a medline was performed with the key words "placenta transfer of..." followed by the name of a single antiviral and it was repeated for 20 antivirals. Thirdly, another medline was performed using the following key words "pharmacokinetics of antiviral in newborn" in order to collect those articles which describe in vivo transfer of antivirals. The literature was critically read and a written note was produced. RESULTS The literature on the placental transfer of antivirals includes studies in vitro perfusing the human placenta and studies performed in vivo in which the cord and maternal antiviral plasma concentrations are compared. Both the results obtained in vitro and in vivo show that the protease inhibitors poorly transfer the placenta because of their great molecular weight. With the exception of didanosine, the nucleoside reverse transcriptase inhibitors and nelfinavir, a non-nucleoside reverse transcriptase inhibitor, cross the placenta and the cord, and maternal plasma concentrations equilibrate. CONCLUSIONS In vitro and in vivo results are consistent with the view that the nucleoside reverse transcriptase inhibitors cross the human placenta and produce significant pharmacological concentrations in the fetal circulation. Nevirapine, the only studied non-nucleoside reverse transcriptase inhibitor, reach the equilibrium between the fetal and maternal concentration, whereas the protease inhibitors have a poor transfer across the human placenta.