MUCOSAL INFECTION OF NEONATAL RHESUS-MONKEYS WITH CELL-FREE SIV

Although the mechanisms for maternal transmission are unknown, approxi mately half of the infants congenitally infected with the human immuno deficiency virus type 1 (HIV-1) seem to become infected late in gestat ion or during delivery. Previously, we have developed a rhesus monkey model for congenital infection by injecting cell-free simian immunodef iciency virus (SIV) directly into amniotic fluid. Our results suggeste d that fetal infection may have occurred via skin or mucous membrane e xposure. Mucosal surfaces have also been implicated as a portal of vir us entry by a study in which the presence of serosanguinous fluid in n eonatal gastric aspirates correlated with an increased rate of HIV-1 t ransmission. To test whether cell-free virus could traverse intact neo natal mucosal surfaces, we administered SIVmac251 orally to four rhesu s monkey neonates within 1 hr following cesarean section delivery. All four neonates developed viremia and were positive by cocultivation an d PCR. Seroconversion occurred in three of the four neonates. The SIV dose given was within physiological range as shown by end-point diluti on of virus stock and viremic plasma samples of juvenile rhesus monkey s. This primate model for mucosal transmission of cell-free virus feat ures a high infection rate, thus making studies of mucosal immunity an d the development of strategies to prevent intrapartum virus transmiss ion possible.