Innate immune sensing of DNA viruses

Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA.
Virology (Impact Factor: 3.32). 02/2011; 411(2):153-62. DOI: 10.1016/j.virol.2011.02.003
Source: PubMed


DNA viruses are a significant contributor to human morbidity and mortality. The immune system protects against viral infections through coordinated innate and adaptive immune responses. While the antigen-specific adaptive mechanisms have been extensively studied, the critical contributions of innate immunity to anti-viral defenses have only been revealed in the very recent past. Central to these anti-viral defenses is the recognition of viral pathogens by a diverse set of germ-line encoded receptors that survey nearly all cellular compartments for the presence of pathogens. In this review, we discuss the recent advances in the innate immune sensing of DNA viruses and focus on the recognition mechanisms involved.

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    • "After viral recognition, the levels of MDA5 and LGP2 increase, and this promotes accumulation of Mx. When the PRRs detect pathogen invasion, signal transduction processes induce cells of the innate immune system to produce IFNs and hormones (Rathinam and Fitzgerald, 2011). A recent study indicated that myeloid differentiation factor 88 (MyD88), Toll/interleukin-1 receptor domain-containing adapter protein (TRIF) inducing interferon-b and TNF-a occur in grouper, and that these factors interact with TLR22 to promote downstream pathways in anti-pathogen responses (Ding et al., 2012). "
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    ABSTRACT: Betanodoviruses cause viral nervous necrosis in numerous fish species, but some species are resistant to infection by these viruses. It is essential to fully characterize the immune responses that underlie this protective response. Complete characterization of the immune responses against nodaviruses may allow the development of methods that stimulate fish immunity and of an effective betanodavirus vaccine. Such strategies could include stimulation of specific immune system responses or blockage of factors that decrease the immune response. The innate immune system clearly provides a front-line defense, and this includes the production of interferons and other cytokines. Interferons that are released inside infected cells and that suppress viral replication may be the most ancient form of innate immunity. This review focuses on the immune responses of fish to betanodavirus infection.
    Developmental and comparative immunology 04/2014; 43(2):174-183. DOI:10.1016/j.dci.2013.07.019 · 2.82 Impact Factor
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    • "The host proteins that sense viral PAMPs, termed pattern recognition receptors (PRRs), range in their specific targets enormously and are located in endosomes and the cell cytosol (2–4). Some important PRRs that are specific to virus nucleic acid recognition include Toll-Like Receptors (TLRs) TLR3, TLR7, TLR8, and TLR9 (4, 5). Absent in Melanoma 2 (AIM2)-like receptors such as the AIM2 inflammasome and IFI16 (6–9), and RIG-I-like receptors including MDA5 (melanoma differentiation associated gene 5) and RIG-I (retinoic acid inducible gene I) (10, 11). "
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    ABSTRACT: Interferon-induced proteins with tetratricopeptide repeats (IFITs) are a family of proteins, which are strongly induced downstream of type I interferon signaling. The molecular mechanism of IFIT anti-viral activity has been studied in some detail, including the recently discovered direct binding of viral nucleic acid, the binding to viral and host proteins, and the possible involvement in anti-viral immune signal propagation. The unique structures of some members of the IFIT family have been solved to reveal an internal pocket for non-sequence-specific, but conformation- and modification-specific, nucleic acid binding. This review will focus on recent discoveries, which link IFITs to the anti-viral response, intrinsic to the innate immune system.
    Frontiers in Immunology 03/2014; 5:94. DOI:10.3389/fimmu.2014.00094
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    • "It has been reported that IFI16 activates inflammasome upon human herpes virus 8 and Epstein-Barr virus infection [82] [93]. Unlike absent in melanoma 2 (AIM2), a cytosolic DNA receptor that activates inflammasome in the cytoplasm [91], IFI16 senses the human herpes virus 8 genome and assembles a functional inflammasome in the nucleus, resulting in caspase-1 activation and processing of IL-1β in the cytoplasm. Therefore, IFI16 mediates not only type I IFN induction but also inflammasome activation. "
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    ABSTRACT: Herpes simplex viruses (HSV) are human pathogens that establish lytic and latent infections. Reactivation from latency occurs intermittently, which represents a life-long source of recurrent infection. In this complex process, HSV triggers and neutralizes innate immunity. Therefore, a dynamic equilibrium between HSV and the innate immune system determines the outcome of viral infection. Detection of HSV involves pathogen recognition receptors which include Toll-like receptors (TLRs), retinoic acid-inducible gene I (RIG-I) like receptors, and cytosolic DNA sensors. Moreover, innate components or pathways exist to sense membrane fusion upon viral entry into host cells. Consequently, this surveillance network activates downstream transcription factors, leading to the induction of type I interferon (IFN) and inflammatory cytokines. Not surprisingly, with the capacity to establish chronic infection HSV has evolved strategies that modulate or evade innate immunity. In this review, we describe recent advances pertinent to the interplay of HSV and the induction of innate immunity mediated by pathogen recognition receptors or pathways.
    Journal of Molecular Biology 11/2013; 426(6). DOI:10.1016/j.jmb.2013.11.012 · 4.33 Impact Factor
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