HIV-1 has been known to infect a variety of non lymphoid cell lines, where the mode of entry has been postulated to involve an additional or an independant receptor or a second messenger-like molecule. The extent of viral replication in these cell lines is vastly different from productive to abortive infections suggestive of host dependant controls on viral replication. These model systems are ideal for identification of cellular and viral factors involved in relication. Also, in some instances, certain epithelial cells from patients ( e.g colon, cervical etc) have been shown to harbor viral nucleic acid. Recent epidemiologic studies suggest that some transmission to the fetus may occur in utero and may involve infection of non lymphoid cell types. We have initiated studies to explore mechanisms of active or possibly abortive viral infections in these cell types. The target cells we have chosen to work with are neuroblastoma cell lines SKNSH, SKNMC, a human embryonic cell line, L132, two cervical cell lines SiHa and C33A, two uterine cell lines HS 825T and HS 258T and a vaginal cell line HS 769 Vg. These cell lines have been infected with HIV-1 and the course of infection is being monitored. The kinetics of viral replication assessed by synthesis of viral DNA, RNA and proteins is being analyzed in these cell lines. Cellular factors such as NFkB, NFAT, c-fos/jun, kinases, methylases and cytokines that may govern the different extents to which viral replication occurs in these different cell lines will be investigated.
