SIVagm infection of its natural African green monkey host.
Possible reasons for the apathogenicity of simian immunodeficiency virus (SIVagm) in its natural African green monkey (AGM) host were investigated. In most respects, the SIVagm/AGM system was shown to resemble human immunodeficiency virus type 1 (HIV-1) infection of humans. AGMs were shown to respond to infection with immune responses similar to those seen in HIV-1-infected humans, with no obvious controlling mechanism observed. The rate of SIVagm in vivo variability was likewise shown to be consistent with that described for HIV-1. Similarly, the level of infection in the peripheral blood was reminiscent of the level in asymptomatic HIV-1-infected patients, although never reaching the levels associated with AIDS. Some potentially important differences were, however, observed. Like humans, AGM CD8+ cells secrete a factor able to suppress SIVagm (and HIV-1) replication but unlike humans, AGMs have a very high percentage of CD8+ lymphocytes in circulation. Also, unlike humans during the asymptomatic stages of infection, AGM lymph nodes do not seem to act as a reservoir for SIVagm and the lymph node structure is not affected. Whether these phenomena are causative or incidental to the state of apathogenicity is the subject of further investigations.
Norley
S G
SG
Paul-Ehrlich-Institut, Langen, Germany.
D000818:Animals; D002522:Chlorocebus aethiops; D007113:Immunity, Innate; D016097:Simian Acquired Immunodeficiency Syndrome / Q000276:immunology*; D015302:Simian Immunodeficiency Virus / Q000276:immunology*