Journal of Virology, February 2001, p. 1533-1539, Vol. 75, No. 3
0022-538X/01/$04.00+0 DOI: 10.1128/JVI.75.3.1533-1539.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Divisions of Microbiology and Immunology1 and Research Resources,3 Yerkes Regional Primate Research Center, and Departments of Microbiology2 and Pathology,5 Emory University, and Retroviral Diseases Branch, DASTLR, Centers for Disease Control and Prevention,4 Atlanta, Georgia
Received 30 May 2000/Accepted 24 October 2000
To investigate the pathogenicity of a virus originating in a chimpanzee with AIDS (C499), two chimpanzees were inoculated with a plasma-derived isolate termed human immunodeficiency virus type 1NC (HIV-1NC). A previously uninfected chimpanzee, C534, experienced rapid peripheral CD4+ T-cell loss to fewer than 26 cells/µl by 14 weeks after infection. CD4+ T-cell depletion was associated with high plasma HIV-1 loads but a low virus burden in the peripheral lymph node. The second chimpanzee, C459, infected 13 years previously with HIV-1LAV, experienced a more protracted course of peripheral CD4+ T-cell loss after HIV-1NC inoculation, resulting in fewer than 200 cells/µl by 96 weeks postinoculation. The quantities of viral RNA in the plasma and peripheral lymph node from C459 were below the lower limits of detection prior to inoculation with HIV-1NC but were significantly and persistently increased after superinfection, with HIV-1NC representing the predominant viral genotype. These results show that viruses derived from C499 are more pathogenic for chimpanzees than any other HIV-1 isolates described to date.
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