The HIV Life Cycle

The HIV life cycle includes several crucial steps, starting from the attachment of the virus to the host cell membrane and finishing with the release of progeny virions from the cell. The HIV replication cycle can be summarized in six steps. These steps include (1) binding and entry, (2) uncoating, (3) reverse transcription, (4) provirus integration, (5) virus proteins synthesis and assembly and (6) budding which represent in figure 1.

The entry pathway of HIV-1 and HIV-2 can be divided into three major events: virus binding to the cell, activation and fusion. The HIV-1 envelope (Env) protein was encodes from Env gene which mediates virus entry into target cells. The Env in post-translation step is cleaved by the cellular protease to produce

Through the reverse transcription, the viral RNA is transcribed to viral double-stranded DNA. This process is catalyzed by an RNA-dependent DNA polymerase, also known as reverse transcriptase, which is encoded by the viral genome, which is integrated within the cell genome by integrase. This protein cleaves nucleotides of each 3’ ends of the double helix DNA creating two sticky ends, transfers the modified provirus DNA into the cell nucleus and facilitates its integration into the host genome. The integration of proviral DNA and the expression of the provirus require that target cell is in an activated state. Monocytes/macrophages, microglial cells, and latently infected quiescent CD4+ T-cells contain integrated provirus and are important long-living cellular reservoirs of HIV. Upon cell activation, transcription of proviral DNA into a messenger RNA occurs. Transcription process initially results in the early synthesis of regulatory HIV-1 proteins such as Tat and Rev. Tat binds to the TAR site (Transactivation Response Element) at the beginning of the HIV-1 RNA in the nucleus and stimulates the transcription and the formation of longer RNA transcripts. Rev facilitates the transcription of longer RNA transcripts and the expression of structural and enzymatic genes and inhibits the production of regulatory proteins, therefore promoting the formation of mature viral