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Replicative fitness of transmitted HIV-1 drives acute immune activation, proviral load in memory CD4+ T cells, and disease progression. 2015
Daniel T Claiborne, and
Jessica L Prince, and
Eileen Scully, and
Gladys Macharia, and
Luca Micci, and
Benton Lawson, and
Jakub Kopycinski, and
Martin J Deymier, and
Thomas H Vanderford, and
Krystelle Nganou-Makamdop, and
Zachary Ende, and
Kelsie Brooks, and
Jianming Tang, and
Tianwei Yu, and
Shabir Lakhi, and
William Kilembe, and
Guido Silvestri, and
Daniel Douek, and
Paul A Goepfert, and
Matthew A Price, and
Susan A Allen, and
Mirko Paiardini, and
Marcus Altfeld, and
Jill Gilmour, and
Eric Hunter
Emory Vaccine Center, Yerkes National Primate Research Center, Emory University, Atlanta, GA 30329;
HIV-1 infection is characterized by varying degrees of chronic immune activation and disruption of T-cell homeostasis, which impact the rate of disease progression. A deeper understanding of the factors that influence HIV-1-induced immunopathology and subsequent CD4(+) T-cell decline is critical to strategies aimed at controlling or eliminating the virus. In an analysis of 127 acutely infected Zambians, we demonstrate a dramatic and early impact of viral replicative capacity (vRC) on HIV-1 immunopathogenesis that is independent of viral load (VL). Individuals infected with high-RC viruses exhibit a distinct inflammatory cytokine profile as well as significantly elevated T-cell activation, proliferation, and CD8(+) T-cell exhaustion, during the earliest months of infection. Moreover, the vRC of the transmitted virus is positively correlated with the magnitude of viral burden in naive and central memory CD4(+) T-cell populations, raising the possibility that transmitted viral phenotypes may influence the size of the initial latent viral reservoir. Taken together, these findings support an unprecedented role for the replicative fitness of the founder virus, independent of host protective genes and VL, in influencing multiple facets of HIV-1-related immunopathology, and that a greater focus on this parameter could provide novel approaches to clinical interventions.
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Benton Lawson, and
Jakub Kopycinski, and
Martin J Deymier, and
Thomas H Vanderford, and
Krystelle Nganou-Makamdop, and
Zachary Ende, and
Kelsie Brooks, and
Jianming Tang, and
Tianwei Yu, and
Shabir Lakhi, and
William Kilembe, and
Guido Silvestri, and
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Paul A Goepfert, and
Matthew A Price, and
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