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

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 watch over of infection.. specialists on the leading edge of those parts supply serious tests with reference to influenza virology, immunology, mobile and molecular biology, and pathogenesis. quantity I offers overviews of the newest findings on molecular determinants of viral pathogenicity, virus access and mobile tropism, pandemic hazard evaluate, transmission and pathogenesis in animal species, viral evolution, ecology and antigenic version, whereas quantity II makes a speciality of the function of innate and adaptive immunity in pathogenesis, improvement of vaccines and antivirals.

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Additional info for Influenza Pathogenesis and Control - Volume II

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2011; Lupfer et al. 2013). Together, these findings suggest that NLRs execute differential role in response to influenza virus infection to obtain a balanced innate immunity. 1 Cytokines and Chemokines These mainly activate and attract various immune cells to the site of infection. Type I IFNs are the principal antiviral effectors to inhibit viral replication, and also promote greater activation of innate immune cells, particularly DCs, to facilitate the induction of adaptive immunity. 2 Soluble Innate Mediators These function mainly by direct interaction with the virus outside the cells, resulting in either inhibition of viral binding to target cells, or in disruption of viral membranes (reviewed in Tripathi et al.

2009). It is not clear whether the reduced number of NK cells in peripheral blood is a reflection of augmented recruitment of NK cells to the site of infection, the respiratory tract. However, the fatal cases of influenza virus infections showed reduced number or absence of NK cells in lung inflammatory infiltrate (Denney et al. 2010; Welliver et al. 2007). Consistent with this, studies have found that influenza virus-infection of NK cells inhibits their functions of cytotoxicity and cytokine and chemokine secretion in humans (Mao et al.

S. Maddur lo + DC-SIGNhi CD11b+ CD11c+ CD11clo Plasmacytoid DCs (pDCs) CD11b Ly6C CD11c+ hi/lo Monocyte-derived DCs CD141 CD11c mDC2 hi CD11chi cDCs CD103+ CD11blo CD1c+ CD11chi mDC1 CD11c cDCs HLA-DR+ CD123hi CD11b- MHCIIlo CD11b- LyC6+ mPDCA-1+ hi CD14- CD1chi DC-SIGN + CX3CR1int SIRPa+ Mar-1 CD1a+ CD64+ + CD11blo CLEC9a CD24hi CD64 XCR1+ CLEC9a+ - SIRPa- Langerin- CD1a+ SAa2,6 [ SAa2,3 MGL MMR DC-SIGN SAa2,6 [ SAa2,3 SAa2,6 [ SAa2,3 MMR (mDC1) TLR7 TLR4 NLRP3 RIG-I TLR3 TLR4 RIG-I TLR3 TLR4 RIG-1 Langerin+/- Virus sensing receptors TLR3 SAa2,6 [ SAa2,3 Virus binding receptors CD11blo SIRPa+ XCR1+ Langerin+ CD24lo Langerin- CD64- CX3CR1 int SIRPa+ CD11bhi CD103- hi MHCIIhi Dentritic cells (DCs) HLA-DRhi Phenotype markers Mice Humans Cell type Table 1 (continued) IL-6 IFN-a (high) TNFa IL-12 IL-6 TNFa IL-6 CXCL10 TNFa IL-12 IL-6 IFN-a (low) Innate response + +++ ++ +++ Degree of productive infection : NC : : : ; : : (continued) Kaminski et al.

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