Regulation of HIV-1 infectivity and pathogenesis of AIDS remain central interests of the laboratory. Unlike the typical animal-oncoretroviruses, lentiviruses such as HIV have the ability to infect and replicate within non-cycling cells.  Nucleo-cytoplasmic transport of the viral genome is vital for the replication and assembly of many viruses. Nuclear transport of Human immunodeficiency viral  (HIV) genome, for instance, is critical for productive infection in non-dividing cells such as human macrophages.  Our understanding on the nuclear import of HIV preintegration complexes into the nucleus of non-dividing cells remains rudimentary, and identification of cellular protein(s) which interact with viral PICs is eagerly awaited and will reveal cellular system that are important to diverse and basic cellular processes. Our laboratory will focus on two issues: mechanism of HIV PICs nuclear import, and signals in PICs that regulate its nuclear import.  To achieve this goal we will clone and characterize the host genes that are involved in this process.  We will also attempt to identify how the host genes interact with viral proteins to bring about the events of HIV pathogenesis.  Furthermore, a better understanding of nuclear transport during viral infection might prove useful for designing antiviral therapies and for designing delivery vectors for gene therapy, which is a rapidly developing and increasingly important area of research in biomedical sciences. 


HIV and Host cell cycle regulation: