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• W2483609541 abstract "Hosts have evolved highly sophisticated mechanisms to prevent and control viral infections. These include the innate immune response, hardwired into most eukaryotic cells and triggered soon after virus entry, as well as the more specialized adaptive immune response, defined by aspects of antigen specificity and memory. Following host cell infection, most viruses trigger one or more pattern recognition receptors, which have evolved to recognize virus-specific signatures, or pathogen associated molecular patterns (eg, 5′-triphosphate RNA), and upon ligand binding, trigger conserved signaling pathways that culminate in the functional activation of critical host transcription factors involved in the initiation of various antiviral responses. Several virus stress-induced genes (vSIGs) are transcribed as a result of this early activation, including those encoding the secretory type I and III interferons (IFNs). Expression and secretion of IFNs result in their binding to cognate surface receptors on cells in both autocrine and paracrine patterns, followed by ligand-stimulated activation of the JAK-STAT signaling cascade. Activated STATs, together with other accessory factors, then translocate to the nucleus and initiate a second wave of transcription—resulting in the expression of hundreds of genes that encode antiviral proteins targeting multiple aspects of viral replication, assembly, maturation, and spread. This second phase of the IFN response is also crucial for ensuring that initial IFN expression is amplified through positive feedback, thus ensuring robust establishment of an antiviral state in different host cell types, both infected and uninfected. Coevolution of hosts and their viruses [also known as the Red Queen Hypothesis (Muraille, 2013)] likely resulted not only in the present complexity of the host innate response, but also in the emergence of viral strategies to block the innate response at multiple steps in order to ensure evolutionary advantage (Medzhitov and Janeway, 1997). Accordingly, most pathogenic viruses, including the rotaviruses, encode factors that target redundant steps of the IFN induction and amplification signaling pathways." @default.
• W2483609541 created "2016-08-23" @default.
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• W2483609541 date "2016-01-01" @default.
• W2483609541 modified "2023-09-27" @default.
• W2483609541 title "Innate Immune Responses to Rotavirus Infection" @default.
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• W2483609541 doi "https://doi.org/10.1016/b978-0-12-802241-2.00012-2" @default.
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