Mycobacterium bovis Bacille Calmette-Guérin Enhances Pathogenicity of Simian Immunodeficiency Virus Infection and Accelerates Progression to AIDS in Macaques: A Role of Persistent T cell Activation in AIDS Pathogenesis
作者： David Lee-Parritz , Prabhat K. Sehgal , Meredith Simon , Dejiang Zhou , Laura Chalifoux
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摘要: It has recently been proposed that Mycobacterium tuberculosis may enhance the pathogenicity of HIV infections and accelerate course disease. This hypothesis tested in present study using a simian immunodeficiency virus macaques (SIVmac)/Mycobacterium bovis bacille Calmette-Guerin (BCG)-coinfected macaque model. Naive chronically SIVmac-infected monkeys were evaluated. Following BCG inoculation, exhibited dominant responses TCR-beta complementarity-determining region 3-restricted T cell subpopulations. BCG-driven activation correlated with marked increase viral loads monkeys. Moreover, prolonged coincided enhanced decline CD4+ PBL counts accelerated progression to clinical AIDS coinfected monkeys, suggesting Mycobacterium-driven be mechanism underlying infection individuals. Within 2 7 mo after coinfection, all died from SIV-induced including tuberculosis-like Surprisingly, naive manifested activation-related toxic shock syndrome profound depletion lymphocytes wk simultaneous SIVmac/BCG inoculation. These animals evidence persistent SIV p27 antigenemia SIVmac-induced In contrast, normal not infected SIVmac survived infection; control showed natural chronic infection. Thus, results this SIV/BCG coinfection model strongly support active can impact remarkably on virus-induced
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