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

细胞凋亡被认为是细胞死亡的生理形式。在与细胞凋亡相关的刺激物中，有哺乳动物DNA和RNA病毒的感染。作为其抗病毒防御的一部分，细胞可以通过产生干扰素（IFN）和/或经历早期凋亡来对病毒攻击作出反应，以防止子代病毒的产生和传播。因此，为了实现成功的复制，某些病毒已经进化出抑制感染细胞产生IFN和/或分别在感染的早期和晚期抑制/诱导细胞凋亡的机制，这是病毒-宿主相互作用的复杂性的基础。我们的建议将研究病毒和宿主先天免疫和凋亡机制之间的相互作用。这将有助于理解病毒复制和发病机制，作为一个模型，马动脉炎病毒，动脉病毒科的原型，在命令巢病毒。与病毒-宿主相互作用主题相关的另一个但重要的目标是鉴定可能在病毒复制中起作用的宿主细胞蛋白。

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.