Abstract

A new human retrovirus, HIV-2, serologically distinct from human immunodeficiency virus type 1 (HIV-1), was first reported in 1985 and isolated in 1986 from 2 AIDS patients from Guinea-Bissau and Cape Verde Islands. Findings related to the characterization of HIV-2 antigenic and immunogenic sites that stimulate strain and type-cross-reactive immunity are illustrated; data from preliminary studies of simian immunodeficiency virus (SIV) are presented; and epidemiological and biological characteristics of HIV-2 infection are also reviewed. Prevention of HIV-2 and SIVsm infection has been achieved in cynomolgus macaques by passive transfer of an anti-SIVsm serum pool with high antibody titres. The identification of antibody-binding regions of HIV is critical for vaccine development studies. The presence of highly immunogenic domains in the extracellular proteins of HIV-2 has also been demonstrated by Western blot analysis using bacterially expressed contiguous segments representing the HIV-2 envelope products. Over 95% of HIV-2 positive sera from Senegal reacted with these protein segments. The antibody-reactive peptide scanning method defined 8 distinct antibody-binding sites in the transmembrane protein gp36 of the HIV-2 strain ROD in addition to the highly immuno-dominant site present at the amino terminus of gp36. Antibody reactions of SIVm-infected macaque sera against selected SIVm envelope peptides were very similar to those of HIV-2 and HIV-1-infected human sera to the corresponding linear antigenic sites, indicating the existence of immunological parallelism between human and simian lentiviruses. HIV-2-induced immunity in inoculated macaques has been shown to protect against SIV-associated disease, indicating that the 2 viruses share group-specific protective immunity. In a study of human sera, the occurrence of an intertype cross-reacting V3-region-specific activity correlated with the presence of cross-neutralizing activity in sera. These findings indicate that the V3 region may be an important neutralizing site not only in HIV-1 but also in HIV-2.

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