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 independent receptor or a second messenger-like molecule. The extent of viral replication in these cell lines is vastly different ranging 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 viral replication. In order to investigate this the target cell we have chosen to work are SKNSH, SKNMC (neuroblastoma cell lines), HTB-14 (derived from an astrocytoma), A-204 and RD114 (rhabdomyosarcoma), A1N4, a normal breast line, MCF-7, BT-20 and BT 483 mammary carcinoma cell lines, TE85 and SAOS-2, 2 osteogenic sarcoma cell lines and L132, a human embryonic cell line. Some of these cell lines have been infected with both HIV-1 and HIV-2. The kinetics of viral replication (assessed by synthesis of viral integrated and unintegrated DNA, RNA and proteins) is being analyzed in these cell lines. Both viral and cellular factors, such as kinases, DNA binding proteins and cytokines, that may govern the different extents to which viral replication occurs in these different cell lines will be investigated at the RNA and protein level.
