AIDS Res Hum Retroviruses. 1997 May 20;13(8):635-45. Unique Identifier :
By animal-to-animal passage in macaques we derived a pathogenic chimeric
simian-human immunodeficiency virus (SHIV) that caused CD4+ T cell loss
and AIDS in pigtail macaques and used it to inoculate 20 rhesus and
pigtail macaques by the intravaginal and intravenous routes. On the
basis of the outcome of infection and patterns of CD4+ T cell loss and
viral load, disease was classified into four patterns: acute, subacute,
chronic, and nonprogressive infection. During the study period, 15 of
the 20 animals developed fatal disease, including AIDS, encephalitis,
pneumonia, and severe anemia. Opportunistic pathogens identified in
these animals included Pneumocystis, cytomegalovirus, Cryptosporidium,
Toxoplasma, and Candida. No single parameter by itself predicted
outcome, although a combination of low CD4+ T cell counts in blood, high
plasma virus levels, and presence of autoantibodies to red blood cells
reliably predicted a fatal outcome. Five animals (25%) died within 3
months of inoculation and constituted the group with acute disease,
whereas the nine animals (45%) with subacute disease died between 3 and
8 months postinoculation. This 70% mortality within 8 months is
significantly shorter than in HIV-1-infected human beings, of whom 70%
develop fatal disease a decade after infection. SHIV infection in
macaques provides a useful model with which to evaluate antiviral
strategies, combining all the advantages of the SIVmac system, yet using
a virus bearing the envelope gene of HIV-1.
*Acquired Immunodeficiency Syndrome/ETIOLOGY *Disease Models, Animal
*HIV-1/GENETICS *Macaca mulatta/VIROLOGY *Macaca nemestrina/VIROLOGY
*SIV/GENETICS