Abstract

This chapter focuses on the study of viral immune evasion. Most viruses spread from one host to the next via secreted bodily fluids; to gain access to their target cells for replication they need to cross epithelial barriers, which can be considered the first line of host defense. Host cell apoptosis is triggered by cell stress signals responding to the virus' attempt to co-opt cellular machinery. Pattern recognition receptors (PRRs) recognize viral components and elicit cytokines and chemokines, which in turn recruit natural killer (NK) cells. Natural killer (NK) cells are an essential component of the first line of defense against viruses. NK cells have two antiviral mechanisms, cytotoxicity and cytokine secretion, and they are the main source of INF-g early in infection. Viral genes that interfere with the MHCI pathway of antigen presentation to CD8 T cells were the first viral immune evasion genes to be described. Specific deletion of viral immune evasion genes has revealed the extraordinary potency of innate immune responses compared to the modest impact of the sophisticated adaptive immune system. However, all viral immune evasion genes, whether they are absolutely required for host species infection or confer a barely perceptible benefit, have been selected by the same balancing evolutionary pressures: the ability of a virus to propagate its genome within a host, the ability to spread to a new host, and the need to maintain a supply of new hosts.

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