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Special Issue "Antiviral Innate Immunity"

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A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Antivirals & Vaccines".

Deadline for manuscript submissions: closed (28 February 2011)

Special Issue Editor

Guest Editor
Prof. Dr. John Guatelli

Division of Infectious Diseases, School of Medecine, University of California, San Diego, 9500 Gilman Drive # 0679 La Jolla, CA 92093, USA
Website | E-Mail

Special Issue Information

Dear Colleagues,

The innate immune response to viruses begins with the detection of viruses by the host, followed by the induction of cellular and molecular effectors with broad antiviral activity. Classically, effectors of the innate response include natural killer cells and the “antiviral state” induced by type I interferons. More recently, a number of intrinsic antiviral host proteins have been identified, including the so-called “restriction factors” that inhibit the replication of members of the retrovirus and other virus families. These factors have in some cases been linked to the innate response, specifically via their induction by interferon. Active issues in the field of antiviral innate immunity include the molecular and cellular mechanisms by which viruses are detected, the identification of new effectors of innate immunity including antiviral proteins and microRNAs, and the mechanisms by which viruses evade and antagonize the innate response. New functional screens and molecular genetic approaches are being used to explore these issues. These approaches seem likely to reveal novel aspects of the host-pathogen relationship and to dissect how these have affected the evolution of the host and viral genomes. We hope in this issue to capture the scope and flavor of these exciting developments.

Prof. Dr. John Guatelli
Guest Editor

Published Papers (6 papers)

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Review

Open AccessReview Innate Antiviral Response: Role in HIV-1 Infection
Viruses 2011, 3(7), 1179-1203; doi:10.3390/v3071179
Received: 24 May 2011 / Revised: 28 June 2011 / Accepted: 29 June 2011 / Published: 14 July 2011
Cited by 16 | PDF Full-text (335 KB)
Abstract
As an early response to infection, cells induce a profile of the early inflammatory proteins including antiviral cytokines and chemokines. Two families of transcriptional factors play a major role in the transcriptional activation of the early inflammatory genes: The well-characterized family of NFkB
[...] Read more.
As an early response to infection, cells induce a profile of the early inflammatory proteins including antiviral cytokines and chemokines. Two families of transcriptional factors play a major role in the transcriptional activation of the early inflammatory genes: The well-characterized family of NFkB factors and the family of interferon regulatory factors (IRF). The IRFs play a critical role in the induction of type I interferon (IFN) and chemokine genes, as well as genes mediating antiviral, antibacterial, and inflammatory responses. Type I IFNs represent critical components of innate antiviral immunity. These proteins not only exert direct antiviral effects, but also induce maturation of dendritic cells (DC), and enhance functions of NK, T and B cells, and macrophages. This review will summarize the current knowledge of the mechanisms leading to the innate antiviral response with a focus on its role in the regulation of HIV-1 infection and pathogenicity. We would like this review to be both historical and a future perspective. Full article
(This article belongs to the Special Issue Antiviral Innate Immunity)
Open AccessReview Systems-Biology Approaches to Discover Anti-Viral Effectors of the Human Innate Immune Response
Viruses 2011, 3(7), 1112-1130; doi:10.3390/v3071112
Received: 9 May 2011 / Revised: 26 June 2011 / Accepted: 29 June 2011 / Published: 11 July 2011
Cited by 4 | PDF Full-text (290 KB)
Abstract
Virus infections elicit an immediate innate response involving antiviral factors. The activities of some of these factors are, in turn, blocked by viral countermeasures. The ensuing battle between the host and the viruses is crucial for determining whether the virus establishes a foothold
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Virus infections elicit an immediate innate response involving antiviral factors. The activities of some of these factors are, in turn, blocked by viral countermeasures. The ensuing battle between the host and the viruses is crucial for determining whether the virus establishes a foothold and/or induces adaptive immune responses. A comprehensive systems-level understanding of the repertoire of anti-viral effectors in the context of these immediate virus-host responses would provide significant advantages in devising novel strategies to interfere with the initial establishment of infections. Recent efforts to identify cellular factors in a comprehensive and unbiased manner, using genome-wide siRNA screens and other systems biology “omics” methodologies, have revealed several potential anti-viral effectors for viruses like Human immunodeficiency virus type 1 (HIV-1), Hepatitis C virus (HCV), West Nile virus (WNV), and influenza virus. This review describes the discovery of novel viral restriction factors and discusses how the integration of different methods in systems biology can be used to more comprehensively identify the intimate interactions of viruses and the cellular innate resistance. Full article
(This article belongs to the Special Issue Antiviral Innate Immunity)
Open AccessReview The Natural Killer Cell Cytotoxic Function Is Modulated by HIV-1 Accessory Proteins
Viruses 2011, 3(7), 1091-1111; doi:10.3390/v3071091
Received: 14 June 2011 / Revised: 23 June 2011 / Accepted: 24 June 2011 / Published: 8 July 2011
Cited by 12 | PDF Full-text (528 KB)
Abstract
Natural killer (NK) cells’ major role in the control of viruses is to eliminate established infected cells. The capacity of NK cells to kill virus-infected cells is dependent on the interactions between ligands on the infected cell and receptors on the NK cell
[...] Read more.
Natural killer (NK) cells’ major role in the control of viruses is to eliminate established infected cells. The capacity of NK cells to kill virus-infected cells is dependent on the interactions between ligands on the infected cell and receptors on the NK cell surface. Because of the importance of ligand-receptor interactions in modulating the NK cell cytotoxic response, HIV has developed strategies to regulate various NK cell ligands making the infected cell surprisingly refractory to NK cell lysis. This is perplexing because the HIV-1 accessory protein Vpr induces expression of ligands for the NK cell activating receptor, NKG2D. In addition, the accessory protein Nef removes the inhibitory ligands HLA-A and -B. The reason for the ineffective killing by NK cells despite the strong potential to eliminate infected cells is due to HIV-1 Vpu’s ability to down modulate the co-activation ligand, NTB-A, from the cell surface. Down modulation of NTB-A prevents efficient NK cell degranulation. This review will focus on the mechanisms through which the HIV-1 accessory proteins modulate their respective ligands, and its implication for NK cell killing of HIV-infected cells. Full article
(This article belongs to the Special Issue Antiviral Innate Immunity)
Open AccessReview RIG-I Like Receptors in Antiviral Immunity and Therapeutic Applications
Viruses 2011, 3(6), 906-919; doi:10.3390/v3060906
Received: 9 April 2011 / Revised: 4 June 2011 / Accepted: 9 June 2011 / Published: 23 June 2011
Cited by 31 | PDF Full-text (315 KB)
Abstract
The RNA helicase family of RIG-I-like receptors (RLRs) is a key component of host defense mechanisms responsible for detecting viruses and triggering innate immune signaling cascades to control viral replication and dissemination. As cytoplasm-based sensors, RLRs recognize foreign RNA in the cell and
[...] Read more.
The RNA helicase family of RIG-I-like receptors (RLRs) is a key component of host defense mechanisms responsible for detecting viruses and triggering innate immune signaling cascades to control viral replication and dissemination. As cytoplasm-based sensors, RLRs recognize foreign RNA in the cell and activate a cascade of antiviral responses including the induction of type I interferons, inflammasome activation, and expression of proinflammatory cytokines and chemokines. This review provides a brief overview of RLR function, ligand interactions, and downstream signaling events with an expanded discussion on the therapeutic potential of targeting RLRs for immune stimulation and treatment of virus infection. Full article
(This article belongs to the Special Issue Antiviral Innate Immunity)
Open AccessReview Pattern Recognition Receptors and the Innate Immune Response to Viral Infection
Viruses 2011, 3(6), 920-940; doi:10.3390/v3060920
Received: 13 April 2011 / Revised: 27 May 2011 / Accepted: 2 June 2011 / Published: 23 June 2011
Cited by 157 | PDF Full-text (362 KB)
Abstract
The innate immune response to viral pathogens is critical in order to mobilize protective immunity. Cells of the innate immune system detect viral infection largely through germline-encoded pattern recognition receptors (PRRs) present either on the cell surface or within distinct intracellular compartments. These
[...] Read more.
The innate immune response to viral pathogens is critical in order to mobilize protective immunity. Cells of the innate immune system detect viral infection largely through germline-encoded pattern recognition receptors (PRRs) present either on the cell surface or within distinct intracellular compartments. These include the Toll-like receptors (TLRs), the retinoic acid-inducble gene I-like receptors (RLRs), the nucleotide oligomerization domain-like receptors (NLRs, also called NACHT, LRR and PYD domain proteins) and cytosolic DNA sensors. While in certain cases viral proteins are the trigger of these receptors, the predominant viral activators are nucleic acids. The presence of viral sensing PRRs in multiple cellular compartments allows innate cells to recognize and quickly respond to a broad range of viruses, which replicate in different cellular compartments. Here, we review the role of PRRs and associated signaling pathways in detecting viral pathogens in order to evoke production of interferons and cytokines. By highlighting recent progress in these areas, we hope to convey a greater understanding of how viruses activate PRR signaling and how this interaction shapes the anti-viral immune response. Full article
(This article belongs to the Special Issue Antiviral Innate Immunity)
Open AccessReview Antiviral Inhibition of Enveloped Virus Release by Tetherin/BST-2: Action and Counteraction
Viruses 2011, 3(5), 520-540; doi:10.3390/v3050520
Received: 18 March 2011 / Revised: 19 April 2011 / Accepted: 28 April 2011 / Published: 6 May 2011
Cited by 38 | PDF Full-text (596 KB)
Abstract
Tetherin (BST2/CD317) has been recently recognized as a potent interferon-induced antiviral molecule that inhibits the release of diverse mammalian enveloped virus particles from infected cells. By targeting an immutable structure common to all these viruses, the virion membrane, evasion of this antiviral mechanism
[...] Read more.
Tetherin (BST2/CD317) has been recently recognized as a potent interferon-induced antiviral molecule that inhibits the release of diverse mammalian enveloped virus particles from infected cells. By targeting an immutable structure common to all these viruses, the virion membrane, evasion of this antiviral mechanism has necessitated the development of specific countermeasures that directly inhibit tetherin activity. Here we review our current understanding of the molecular basis of tetherin’s mode of action, the viral countermeasures that antagonize it, and how virus/tetherin interactions may affect viral transmission and pathogenicity. Full article
(This article belongs to the Special Issue Antiviral Innate Immunity)

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