ABSTRACT
In 1983, Barre´-Sinoussi et al.1 isolated the human immunodeficiency virus type 1 (HIV-1) and Gallo et al. proved in 1984 that it was the etiologic agent responsible for acquired immunodeficiency syndrome (AIDS).2 HIV-1 and HIV-2 are two cousin types of retroviruses able to infect humans and they both belong to the lentivirus subfamily. While HIV-1 has led to worldwide pandemics, HIV-2 is mostly limited to West Africa and appears to be less pathogenic than HIV-1.3,4
HIV cycle follows the ‘‘classical’’ retroviral cycle with the following steps: (1) binding of the virus to receptors, (2) fusion with the viral core inserted into the cell, (3) reverse transcription of the viral genome, (4) nuclear import of double-stranded DNA, (5) integration of the proviral DNA into the host genomic DNA, (6) transcription of viral RNA and translation of viral proteins, (7) budding of the virus from the cell membrane and maturation, and (8) new cycle of infection of uninfected cells. HIV infects mainly the CD4þ cells of the immune system and cells from the reticulo-endothelial system such as macrophages. Once integrated in the genome, the provirus behaves essentially as a cellular gene and can be reactivated following an immune stimulation linked to undercurrent infections or to stress.5-7
The time span between the HIV-1 initial infection and the appearance of disease symptoms can vary from a few months to several years.
