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The outcome of noncytolytic viral infections is largely determined by the cellular immune response. My laboratory focussed on the host-virus interactions that determine the outcome of hepatitis B virus (HBV) and hepatitis C virus (HCV) infections. Using a combination of real time viral dynamics, development of cell-based and animal models of HBV and HCV infection, and quantitative functional T cell analysis of infected humans and subhuman primates and in transgenic mice, we demonstrated a direct relationship between viral clearance and the vigor, kinetics and homing potential of the antiviral T cell response to HBV and HCV, the rate with which they spread after inoculation, their ability to escape immune recognition, and the host and viral mechanisms that determine viral clearance and persistence and the development of hepatocellular carcinoma. In the course of those studies we discovered that virus-specific T cells can suppress viral replication noncytolytically by secreting antiviral cytokines that can purge viruses from infected cells without killing them, i.e. a third effector limb in the immune response besides antibody neutralization and T cell-mediated destruction of infected cells. This led to studies that identified the intracellular antiviral effector pathways that are triggered by these cytokines, pinpointed the steps in the viral life cycles that are targeted by the cytokines, and defined the mechanisms deployed by the viruses to defeat their antiviral effects.
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Jessica Fioravanti,Pietro Di Lucia,Diletta Magini,Federica Moalli,Carolina Boni,Alexandre Pierre Benechet,Valeria Fumagalli,Donato Inverso,Andrea Vecchi, Amleto Fiocchi, Stefan Wieland,Robert Purcell,
semanticscholar(2017)
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ENCYCLOPEDIA OF IMMUNOBIOLOGY, VOL 4: IMMUNITY TO PATHOGENS AND TUMORS (2016)
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