By Peter Palese (Editor), Jean-Pierre Changeux (Editor)
This e-book is a wonderful, up to date reference on a comparatively younger region of analysis during which virology, mobile biology and molecular pathogenesis govern the rules of coinvestigation. hence, the booklet could be of significant curiosity to virologists, molecular immunologists and biologists, and biochemists but additionally to scientific pharmacologists within the long term look for new antiviral brokers. Ulrich Desselberger, Gif-sur-Yvette/Cambridge. an infection of a na?ve (non-immune) host with a scourge elicits a right away reaction which leads to a cascade of alterations within the host, together with an interferon reaction (innate immunity). the end result of this interplay is encouraged by means of the genes of the virus in addition to the genes of the host. curiously, assorted viruses do it in several methods. not just is there a plethora of mechanisms utilized by the invading organisms, however the host has additionally developed a good number of redundant and powerful countermeasures. This interaction of host and virus represents probably the most major frontiers in biology this present day. A clearer realizing of the mechanisms concerned will arm us with higher suggestions to accommodate viruses, together with rising pathogens and power bioterrorism brokers. This booklet is bound to learn scholars, scientists, and physicians operating within the parts of virology, immunology, microbiology, and infectious illnesses. Pharmaceutical execs also will locate curiosity during this illuminating look at virus/host interactions.
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Extra info for Modulation of Host Gene Expression and Innate Immunity by Viruses
More recently, they have been implicated in signaling from both TLRs and the intracellular bacterial sensors, Nod1 and Nod260. The CARD-domain-containing kinase RIP2 has also been implicated in cytokine production, particularly downstream of TLR2, 3, and 4. However, RIG-I is the first CARD-domain signaling molecule directly implicated in IFN production in virus-infected cells. A model for how RIG-I acts as a sensor for cytoplasmic virus replication posits that it acts as an RNA-activated switch.
INTRODUCTION The type I interferons (IFNα and IFNβ) were first characterized as cytokines capable of inducing an antiviral state in sensitive target cells1. They were discovered as a substance produced by virus-infected cells that was capable of conferring protection of uninfected naïve cells from subsequent infection. Since their discovery and characterization as founding members of the type II cytokine family, investigations into IFN biology have served not only to elucidate their potent antiviral properties, but also as a system for understanding molecular mechanisms of gene expression control.
Cell (2001) 106:685-696 17. Ryals J, Dierks P, Ragg H, and Weissmann C, A 46-nucleotide promoter segment from an IFN-alpha gene renders an unrelated promoter inducible by virus. Celll (1985) 41:497507 How Viruses Elicit Interferon Production 31 18. Lopez S, Reeves R, Island ML, Bandu MT, Christeff N, Doly J, and Navarro S, Silencer activity in the interferon-A gene promoters. J. Biol. Chem. (1997) 272:22788-22799 19. Island ML, Mesplede T, Darracq N, Bandu MT, Christeff N, Djian P, Drouin J, and Navarro S, Repression by homeoprotein pitx1 of virus-induced interferon a promoters is mediated by physical interaction and trans repression of IRF3 and IRF7.