HIV-1 replication cycle

Acquired immunodeficiency disease is caused by HIV. HIV types 1 and 2 are members of the Lentivirus genus of the Retroviridae family. HIV-1 is found throughout the world, whereas HIV-2 is still found predominately in West Africa. Although these viruses have replication processes characteristic of the Retroviridae family, marked by single-stranded RNA genome, and replication through reverse transcription and integration, HIV is a new pathogen that seems to have emerged in the twentieth century, likely from cross-species infection from chimpanzees in Africa [1,2]. In contrast to other retroviruses, however, HIV has evolved a variety of accessory genes that can modulate HIV replication. Some of these genes seem to confer abilities to establish persistent infection and to control exuberant replication that may more rapidly cause disease and death in the host. Epidemic HIV infection exploded worldwide in the late 1970s and 1980s. AIDS was described in 1981 [3,4], and HIV was identified and cloned in 1983 [5,6]. Much of the information about the molecular biology of HIV that rapidly accumulated after the cloning of HIV was based on studies with laboratory-derived HIV clones adapted for efficient replication in transformed T-cell lines. Although these experimental systems allowed rapid progress in the understanding of the replication of these newly identified lentiviruses, some of the information obtained from these studies in fact was misleading, because these strains have characteristics and replication properties that are different from those found in most primary HIV strains. In fact, some of these early clones were deficient in some of the;accessory genes or had gene products that exhibited different properties from those in primary strains. An important aspect of HIV replication is the requirement for cellular activation for efficient replication. This activation results in increases in efficiency of reverse transcription, integration, and virus gene expression, in part caused by induction of cellular proteins that are involved in HIV replication. The persistence of HIV replication in individuals in whom chronic infection has established, and the limited effect currently available antiretroviral therapies, make the continued investigation of HIV replication critical for determining potential new targets for novel antiretrovirul therapies.