This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator.
The aim of this pilot study is to establish a GBV-C and SIV coinfection rhesus macaque model for studying the GBV-C and HIV interactions and mechanisms of the potential benefit of GBV-C to slow progression of AIDS. Five Chinese-origin rhesus macaques (Ch Rh) were used in this study. Each animal was inoculated by intravenous route with 10 ml of blood from a human donor containing GBV-C, then 4 months later challenged with plasma from SIVmac239-infected Ch Rh. Seven months after GBV-C inoculation, however, GBV-C was not detected in the plasma of the animals by PCR. All animals were infected with SIV, with a peak viremia in the range of 107 ~ 108 copies/ml at day 14 post infection. Peripheral blood CD4+ T cells had slightly decreased. BrdU labeling was performed to monitor the kinetics of labeled cells to study turnover of lymphocytes and monocytes at the acute phase, and BrdU labeling will be done once during the chronic phase. Data obtained will be analyzed. No significant cellular immune responses were detected by intracellular cytokine staining by flow cytometry during the first 42 days of infection. Taken together, animals were not infected with GBV-C in this experiment which was consistent with observations by others (Jack Stapleton, M.D. Iowa University, personal communication), but contrary to some published studies that showed successful infection in Ch Rh that a different GBV-C genotype was used. It is not known whether or not the use of the different GBV-C genotype is related to the outcome of inoculation. The SIV infection will be monitored, it is expected that new knowledge will be obtained on the dynamics of T cells and virulence of the Ch Rh-adapted SIV during the acute phase of infection.
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