Influenza Pathogenesis and Control - Volume II by Michael B. A. Oldstone, Richard W. Compans PDF

By Michael B. A. Oldstone, Richard W. Compans

ISBN-10: 3319111574

ISBN-13: 9783319111575

ISBN-10: 3319111582

ISBN-13: 9783319111582

This two-volume paintings covers the molecular and phone biology, genetics and evolution of influenza viruses, the pathogenesis of an infection, resultant host innate and adaptive immune reaction, prevention of an infection via vaccination and ways to the healing keep an eye on of infection.. specialists on the leading edge of those components offer serious checks with reference to influenza virology, immunology, telephone and molecular biology, and pathogenesis. quantity I presents overviews of the most recent findings on molecular determinants of viral pathogenicity, virus access and mobile tropism, pandemic hazard evaluation, transmission and pathogenesis in animal species, viral evolution, ecology and antigenic version, whereas quantity II specializes in the function of innate and adaptive immunity in pathogenesis, improvement of vaccines and antivirals.

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2009; Thomas et al. 2009). Strikingly, NLRP3-deficient mice showed collagen deposits in lungs suggesting the delayed resolution of lung injury due to the absence of pro-fibrotic role of IL-1b (Thomas et al. 2009). Notably, the inflammasome complex was found to be dispensable for early clearance (up to 6 days) of the virus (Thomas et al. 2009), but was essential for reducing the viral load in later stage of infection (Allen et al. 2009; Ichinohe et al. 2009). These findings suggested that NLRP3-inflammasome induced inflammatory response, rather than direct viral control, mediates the protective immunity to influenza virus infection, possibly via adaptive immune responses.

2005). Despite neutrophils being important participants in the antiviral response in mouse models, the phenotype and functional relevance of large number of neutrophils that accumulate at the site of infection in influenza virus-infected patients, and their mechanisms of anti viral immunity, are poorly understood. 28 B. S. 3 Macrophages (MU) These include both tissue-resident alveolar macrophages (aMU) as well as recently recruited MU derived from circulating monocytes (moMU) (Table 1). In mouse models, during the course of influenza virus infection, aMU are outnumbered by the migrant monocytes, which differentiate into MU with an activated phenotype (Herold et al.

These findings suggested that NLRP3-inflammasome induced inflammatory response, rather than direct viral control, mediates the protective immunity to influenza virus infection, possibly via adaptive immune responses. NLRC2 (or NOD2) is believed to recognize the viral genomic ssRNA to recruit MAVS adaptor protein to activate IRF3-mediated type I IFN production in DCs and MU in response to influenza virus (Fig. 1). In agreement, NOD2-deficient mice showed decreased type I IFNs and DC activation, and exhibited enhanced susceptibility to lethal dose virus-induced pathogenesis (Lupfer et al.

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Influenza Pathogenesis and Control - Volume II by Michael B. A. Oldstone, Richard W. Compans


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