Cytomegalovirus (CMV) retinitis has become the most common and significant infectious ocular disease associated with the acquired immunodeficiency syndrome (AIDS), affecting approximately 25% of this patient population. While the clinical and histopathologic features of AIDS-associated CMV retinitis have been extensively described, the pathogenic mechanisms involved remain poorly understood. In the previous year we experimentally infected rhesus macaques seropositive for rhesus CMV with two different variants of SIV in an attempt to develop a nonhuman primate model of CMV retinitis. This past year, we have continued to monitor the virological status, both CMV and SIV, along with the health of these macaques for disease manifestations associated with CMV and SIV infection. From these in vivo studies the following observations were made. 1) As we observed last year, experimental infection of rhesus macaques with SIVmac239 or SIV EvT3 did not result in the reactiva tion of CM V in the peripheral blood compartment. These results were unexpected, as studies in HIV-infected patients have shown that human CMV load in the peripheral blood compartment increases prior to clinical signs of CMV retinitis. Thus, our studies support our initial observation that SIV infection alone is insufficient at stimulating widespread CMV dissemination. 2) SIV infection, both EvT3 and SIVmac239, was capable of precipitating the AIDS-like disease in the rhesus macaques, as six of these animals developed significant morbidity associated with other viral pathogens [simian T cell leukemia virus (STLV), and rhesus rhadinovirus (RRV)] and other as yet unidentified pathogens. FUNDING Center-supported project PUBLICATIONS Swanson R, Bergquam E, Wong SW. Characterization of rhesus cytomegalovirus genes associated with anti-viral susceptibility. Virology 240:338-348, 1998.
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