Four subtypes of HIV-1 (M, N, O, and P) likely arose through four separate transmissions of SIV to humans, and the resulting HIV-1 group M strain most commonly infects people worldwide.

[5][6] Therefore, it is theorized that SIV may have previously crossed the species barrier into human hosts multiple times throughout history, but it was not until recently, after the advent of modern transportation and global commuterism, that it finally took hold, spreading beyond localized decimations of a few individuals or single small tribal populations.

Extensive studies in sooty mangabeys have established that SIVsmm infection does not cause any disease in these primates, despite high levels of circulating virus.

Based on molecular clock analyses of sequences, it was previously thought by many that SIV infection in monkeys had happened over the past few hundred years.

[21] In 2008, discovery of an endogenous lentivirus in a prosimian (proto-monkey) primate, the gray mouse lemur native to Madagascar, pushed the origin of SIV-like lentivirus infections in primates back to at least 14 Ma, the last time there was intermingling of mammals between the island of Madagascar and the African mainland, if the infection is attributed to horizontal transmission between homologous hosts.

[22] The SIV virion is a spherical to pleomorphic glycoprotein envelope 110-120 nm across enclosing a 110x50nm truncated cone or wedge-shaped (occasionally rod) capsid containing a dimeric pair of positive-sense single-stranded RNA genomes.

[23] The speed and transcription inaccuracies of RNA viruses give rise to antigenically distinct varieties in a single host animal.

It is postulated that AIDS-like disease in African NHPs represents horizontal transmission of the virus from one or more homologous species in the recent evolutionary past, before equilibrium of co-adaptation has occurred.

Testing wild chimpanzees, researchers detected organ and tissue damage similar to late-stage human AIDS.

[28][27] SIV infected vervets in the wild do not develop chronic immune activation or microbial translocation (assessed by sCD14 as a surrogate biomarker).

[31] In 2012, researchers reported that initial infection of rhesus monkeys by neutralization-resistant SIV strains[32] could be partially prevented through use of an anti-SIVSME543 vaccine obligately including Env protein antigens.

[33] In 2013, a study by a group of authors reported on successful testing of a vaccine containing SIV protein-expressing rhesus cytomegalovirus vector.