The role of structural and nonstructural proteins in the biogenesis of Equine arteritis virus, an aeterivirus

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Apoptosis is considered the physiological form of cell death. Among stimuli that have been associated with cell apoptosis are infections with mammalian DNA and RNA viruses. As part of its antiviral defence, a cell may react to viral aggression through interferon (IFN) production and/or undergoing early apoptosis to prevent production and dissemination of progeny viruses. Thus, to achieve successful replication, certain viruses have evolved mechanisms to suppress the IFN production by the infected cell and/or to suppress/induce apoptosis in early and late stages of infection, respectively, underlying the complexity of virus-host interactions. Our proposal will examine these interactions between viruses and the host innate immunity and apoptotic machinery. This would contribute to the understanding of virus replication and pathogenesis by using, as a model, the Equine arteritis virus, the prototype of the Arteriviridae family within the order Nidovirales. Another but important objective that also is associated to the virus-host interaction topic will be to identify host cell proteins that might be at play in the replication of the virus.