Host and Viral Modulation of RIG-I-Mediated Antiviral Immunity

TY - JOUR

T1 - Host and Viral Modulation of RIG-I-Mediated Antiviral Immunity

AU - Liu, Yiliu

AU - Olagnier, David

AU - Lin, Rongtuan

PY - 2017/1/3

Y1 - 2017/1/3

N2 - Innate immunity is the first line of defense against invading pathogens. Rapid and efficient detection of pathogen-associated molecular patternsviapattern-recognition receptors is essential for the host to mount defensive and protective responses. Retinoic acid-inducible gene-I (RIG-I) is critical in triggering antiviral and inflammatory responses for the control of viral replication in response to cytoplasmic virus-specific RNA structures. Upon viral RNA recognition, RIG-I recruits the mitochondrial adaptor protein mitochondrial antiviral signaling protein, which leads to a signaling cascade that coordinates the induction of type I interferons (IFNs), as well as a large variety of antiviral interferon-stimulated genes. The RIG-I activation is tightly regulatedviavarious posttranslational modifications for the prevention of aberrant innate immune signaling. By contrast, viruses have evolved mechanisms of evasion, such as sequestrating viral structures from RIG-I detections and targeting receptor or signaling molecules for degradation. These virus-host interactions have broadened our understanding of viral pathogenesis and provided insights into the function of the RIG-I pathway. In this review, we summarize the recent advances regarding RIG-I pathogen recognition and signaling transduction, cell-intrinsic control of RIG-I activation, and the viral antagonism of RIG-I signaling.

AB - Innate immunity is the first line of defense against invading pathogens. Rapid and efficient detection of pathogen-associated molecular patternsviapattern-recognition receptors is essential for the host to mount defensive and protective responses. Retinoic acid-inducible gene-I (RIG-I) is critical in triggering antiviral and inflammatory responses for the control of viral replication in response to cytoplasmic virus-specific RNA structures. Upon viral RNA recognition, RIG-I recruits the mitochondrial adaptor protein mitochondrial antiviral signaling protein, which leads to a signaling cascade that coordinates the induction of type I interferons (IFNs), as well as a large variety of antiviral interferon-stimulated genes. The RIG-I activation is tightly regulatedviavarious posttranslational modifications for the prevention of aberrant innate immune signaling. By contrast, viruses have evolved mechanisms of evasion, such as sequestrating viral structures from RIG-I detections and targeting receptor or signaling molecules for degradation. These virus-host interactions have broadened our understanding of viral pathogenesis and provided insights into the function of the RIG-I pathway. In this review, we summarize the recent advances regarding RIG-I pathogen recognition and signaling transduction, cell-intrinsic control of RIG-I activation, and the viral antagonism of RIG-I signaling.

KW - Antiviral

KW - Infection

KW - Innate immunity

KW - RIG-I

KW - Type I IFNs

KW - Virus-host interaction

UR - http://www.scopus.com/inward/record.url?scp=85012069968&partnerID=8YFLogxK

U2 - 10.3389/fimmu.2016.00662

DO - 10.3389/fimmu.2016.00662

M3 - Review

C2 - 28096803

SN - 1664-3224

VL - 7

SP - 662

JO - Frontiers in Immunology

JF - Frontiers in Immunology

IS - JAN

M1 - 662

ER -