ABSTRACT
Lentiviruses related to human immunodeficiency virus type 1 (HIV-1) but not identical, can establish productive infection and cause disease in nonhuman primates. At the molecular level, the simian immunodeficiency viruses (SIV) and related HIV-2 strains have similar genome organization to HIV-1 but are distinct from HIV-1 in many ways (1,2). The TAR regions mediating responses to Tat protein are different in SIV/HIV-2 viruses (3), even though HIV-1 TAR decoys inhibit both SIV and HIV-1 Tat transactivation (4), and there are several differences in the family of accessory genes found roughly in the middle of the virus genome (2). The SU envelope glycoprotein of SIV/HIV-2 lacks a clearly defined V3 loop, and cell tropism determinants are scattered throughout this envelope
gene sequence (5,6), while cell tropism determinants are mainly, but not exclusively, found in the V3 loop of HIV-1 (7-9). The idea has been advanced that SIV/HIV-2 and HIV-1 viruses evolved from a single precursor and that HIV-1 is most closely related to SIVcpz isolated from chimpanzees (10) and may have entered human populations by zoonotic transmission in the course of close contact with nonhuman primate species. The HIV-1 and the SIV/HIV-2 virus families have many similarities, but the viruses are clearly distinct at the sequence level, and the virus families have different genetic maps.
