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      Adenovirus-triggered innate signalling pathways

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          Abstract

          Adenoviruses are important infectious agents and also emerging vectors in different biomedical applications. These viruses elicit a strong innate and adaptive immune response, which influences both the course of disease and the success of the applied vectors. Several Toll-like Receptor (TLR)-dependent and -independent mechanisms contribute to these responses. Understanding of the involved viral and cellular factors is crucial for the treatment of various adenovirus diseases and the optimal design of adenovirus vector applications. Here we summarize our current understanding of the complex nature of adenovirus-induced innate immune mechanisms.

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          Most cited references96

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          Isolation of a common receptor for Coxsackie B viruses and adenoviruses 2 and 5.

          A complementary DNA clone has been isolated that encodes a coxsackievirus and adenovirus receptor (CAR). When transfected with CAR complementary DNA, nonpermissive hamster cells became susceptible to coxsackie B virus attachment and infection. Furthermore, consistent with previous studies demonstrating that adenovirus infection depends on attachment of a viral fiber to the target cell, CAR-transfected hamster cells bound adenovirus in a fiber-dependent fashion and showed a 100-fold increase in susceptibility to virus-mediated gene transfer. Identification of CAR as a receptor for these two unrelated and structurally distinct viral pathogens is important for understanding viral pathogenesis and has implications for therapeutic gene delivery with adenovirus vectors.
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            Pattern recognition receptors TLR4 and CD14 mediate response to respiratory syncytial virus.

            The innate immune system contributes to the earliest phase of the host defense against foreign organisms and has both soluble and cellular pattern recognition receptors for microbial products. Two important members of this receptor group, CD14 and the Toll-like receptor (TLR) pattern recognition receptors, are essential for the innate immune response to components of Gram-negative and Gram-positive bacteria, mycobacteria, spirochetes and yeast. We now find that these receptors function in an antiviral response as well. The innate immune response to the fusion protein of an important respiratory pathogen of humans, respiratory syncytial virus (RSV), was mediated by TLR4 and CD14. RSV persisted longer in the lungs of infected TLR4-deficient mice compared to normal mice. Thus, a common receptor activation pathway can initiate innate immune responses to both bacterial and viral pathogens.
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              Virus-induced Abl and Fyn kinase signals permit coxsackievirus entry through epithelial tight junctions.

              Group B coxsackieviruses (CVBs) must cross the epithelium as they initiate infection, but the mechanism by which this occurs remains uncertain. The coxsackievirus and adenovirus receptor (CAR) is a component of the tight junction and is inaccessible to virus approaching from the apical surface. Many CVBs also interact with the GPI-anchored protein decay-accelerating factor (DAF). Here, we report that virus attachment to DAF on the apical cell surface activates Abl kinase, triggering Rac-dependent actin rearrangements that permit virus movement to the tight junction. Within the junction, interaction with CAR promotes conformational changes in the virus capsid that are essential for virus entry and release of viral RNA. Interaction with DAF also activates Fyn kinase, an event that is required for the phosphorylation of caveolin and transport of virus into the cell within caveolar vesicles. CVBs thus exploit DAF-mediated signaling pathways to surmount the epithelial barrier.
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                Author and article information

                Journal
                1886
                122234
                European Journal of Microbiology and Immunology
                EuJMI
                Akadémiai Kiadó, co-published with Springer Science+Business Media B.V., Formerly Kluwer Academic Publishers B.V.
                2062-509X
                2062-8633
                1 December 2011
                : 1
                : 4
                : 279-288
                Affiliations
                [ 1 ] Max Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany
                [ 2 ] Peninsula College of Medicine and Dentistry, Plymouth, Truro, UK
                [ 3 ] Institute of Molecular Life Sciences, University of Zurich, Zurich, Switzerland
                [ 4 ] Max Planck Institute of Immunobiology and Epigenetics, Stübeweg 51, 79108, Freiburg, Germany
                Author notes
                [* ] +49-761-5108 412, +49-761-5108 403, fejer@ 123456immunbio.mpg.de
                Article
                3
                10.1556/eujmi.1.2011.4.3
                3918130
                24516734
                7098f756-6789-4aab-ad20-f5dcb3b9e01a

                Medicine,Immunology,Health & Social care,Microbiology & Virology,Infectious disease & Microbiology
                viral entry,IRF7,adenovirus,IL-1,type-I interferons,Toll-like receptors,innate response,endosomal escape

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