Human immunodeficiency virus (HIV) is a retrovirus that can lead to a condition in which the immune system begins to fail, leading to opportunistic infections. HIV primarily infects vital cells in the human immune system such as helper T cells (specifically CD4+ T cells), macrophages and dendritic cells. HIV infection leads to low levels of CD4+ T cells through three main mechanisms: firstly, direct viral killing of infected cells; secondly, increased rates of apoptosisin infected cells; and thirdly, killing of infected CD4+ T cells by CD8 cytotoxic lymphocytes that recognize infected cells. When CD4+ T cell numbers decline below a critical level, cell-mediated immunityis lost, and the body becomes progressively more susceptible to opportunistic infections. HIV was classified as a member of the genus Lentivirus, part of the family of Retroviridae. Lentiviruses have many common morphologies and biological properties. Many species are infected by lentiviruses, which are characteristically responsible for long-duration illnesses with a long incubation period. This viral DNA is then integrated into the cellular DNA by a virally encoded integraseso that the genome can be transcribed. Once the virus has infected the cell, two pathways are possible: either the virus becomes latent and the infected cell continues to function, or the virus becomes active and replicates, and a large number of virus particles are liberated that can then infect other cells. HIV2 infections at present, are predominantly found in west Africa where it is the dominant form of HIV. Both HIV1 and HIV2 have the same modes of transmission and are associated with similar opportunistic infections and AIDS. In persons infected with HIV2, immunodeficiency seems to develop more slowly and to be milder, but as the disease advances, HIV2 infectiousness seems to increase. Little is known about the best approach to the clinical treatment and care of patients infected with HIV2. HIV1 and HIV2 have similar gag (viral core) and pol (polymerase) regions, they have relatively dissimilar env (envelope) regions. The resulting complex protrudes from the virus surface as a spike. Retroviral Env protein is not absolutely required for the assembly and release of viral particles, but it does play an active role in these events. It is currently thought that HIV viral entry involves the binding of the viral Env glycoprotein gp120/gp41 to the cell surface receptor CD4, which triggers conformational changes in the envelope proteins. Some of the most genetically diverse regions of the viral genome are present in Env.