The Experts below are selected from a list of 60 Experts worldwide ranked by ideXlab platform

Kin-hang Kok - One of the best experts on this subject based on the ideXlab platform.

  • Suppression of PACT-Induced Type I Interferon Production by Herpes Simplex Virus 1 Us11 Protein
    Journal of virology, 2013
    Co-Authors: Chun Kew, Pak-yin Lui, Chi-ping Chan, Xiang Liu, Ian Mohr, Dong-yan Jin, Kin-hang Kok
    Abstract:

    Herpes simplex virus 1 (HSV-1) Us11 protein is a double-stranded RNA-binding protein that suppresses type I Interferon Production through the inhibition of the cytoplasmic RNA sensor RIG-I. Whether additional cellular mediators are involved in this suppression remains to be determined. In this study, we report on the requirement of cellular double-stranded RNA-binding protein PACT for Us11-mediated perturbation of type I Interferon Production. Us11 associates with PACT tightly to prevent it from binding with and activating RIG-I. The Us11-deficient HSV-1 was indistinguishable from the Us11-proficient virus in the suppression of Interferon Production when PACT was compromised. More importantly, HSV-1-induced activation of Interferon Production was abrogated in PACT knockout murine embryonic fibroblasts. Our findings suggest a new mechanism for viral evasion of innate immunity through which a viral double-stranded RNA-binding protein interacts with PACT to circumvent type I Interferon Production. This mechanism might also be used by other PACT-binding viral Interferon-antagonizing proteins such as Ebola virus VP35 and influenza A virus NS1.

M. Fitzpatrick - One of the best experts on this subject based on the ideXlab platform.

  • Multiplication, Interferon Production and Interferon Sensitivity of Viruses in Dog Kidney Tissue Cultures
    Research in Veterinary Science, 2018
    Co-Authors: R.f. Sellers, M. Fitzpatrick
    Abstract:

    SUMMARY Multiplication, Interferon Production and Interferon sensitivity of a number of viruses were studied in dog kidney tissue cultures. Vaccinia, Bunyamivera, Sendai and horse serum viruses grew well with cytopathic effect, did not produce Interferon but were sensitive to its action. Influenza virus B England multiplied well and gave rise to cytopathic effect, produced Interferon but was insensitive to its action. Influenza A viruses Kunz and Mel, and Semliki Forest virus multiplied poorly but produced Interferon. No multiplication or Interferon Production was found when cultures were infected with bovine enterovirus M6. Contagious canine hepatitis virus, which grew well, did not produce Interferon and was insensitive to its action. Dog kidney Interferon had no effect on virus growth in rhesus monkey or calf kidney tissue cultures, but rhesus monkey kidney Interferon inhibited the growth of dog kidney Interferon-sensitive viruses in dog kidney tissue cultures.

Chun Kew - One of the best experts on this subject based on the ideXlab platform.

  • Suppression of PACT-Induced Type I Interferon Production by Herpes Simplex Virus 1 Us11 Protein
    Journal of virology, 2013
    Co-Authors: Chun Kew, Pak-yin Lui, Chi-ping Chan, Xiang Liu, Ian Mohr, Dong-yan Jin, Kin-hang Kok
    Abstract:

    Herpes simplex virus 1 (HSV-1) Us11 protein is a double-stranded RNA-binding protein that suppresses type I Interferon Production through the inhibition of the cytoplasmic RNA sensor RIG-I. Whether additional cellular mediators are involved in this suppression remains to be determined. In this study, we report on the requirement of cellular double-stranded RNA-binding protein PACT for Us11-mediated perturbation of type I Interferon Production. Us11 associates with PACT tightly to prevent it from binding with and activating RIG-I. The Us11-deficient HSV-1 was indistinguishable from the Us11-proficient virus in the suppression of Interferon Production when PACT was compromised. More importantly, HSV-1-induced activation of Interferon Production was abrogated in PACT knockout murine embryonic fibroblasts. Our findings suggest a new mechanism for viral evasion of innate immunity through which a viral double-stranded RNA-binding protein interacts with PACT to circumvent type I Interferon Production. This mechanism might also be used by other PACT-binding viral Interferon-antagonizing proteins such as Ebola virus VP35 and influenza A virus NS1.

M E Dorf - One of the best experts on this subject based on the ideXlab platform.

  • mapping a dynamic innate immunity protein interaction network regulating type i Interferon Production
    Immunity, 2011
    Co-Authors: Shitao Li, Lingyan Wang, Michael Berman, Youngyun Kong, M E Dorf
    Abstract:

    To systematically investigate innate immune signaling networks regulating Production of type I Interferon, we analyzed protein complexes formed after microbial recognition. Fifty-eight baits were associated with 260 interacting proteins forming a human innate immunity interactome for type I Interferon (HI5) of 401 unique interactions; 21% of interactions were modulated by RNA, DNA, or LPS. Overexpression and depletion analyses identified 22 unique genes that regulated NF-κB and ISRE reporter activity, viral replication, or virus-induced Interferon Production. Detailed mechanistic analysis defined a role for mind bomb (MIB) E3 ligases in K63-linked ubiquitination of TBK1, a kinase that phosphorylates IRF transcription factors controlling Interferon Production. Mib genes selectively controlled responses to cytosolic RNA. MIB deficiency reduced antiviral activity, establishing the role of MIB proteins as positive regulators of antiviral responses. The HI5 provides a dynamic physical and regulatory network that serves as a resource for mechanistic analysis of innate immune signaling.

Xiaojian Wang - One of the best experts on this subject based on the ideXlab platform.

  • rkip and tbk1 form a positive feedback loop to promote type i Interferon Production in innate immunity
    The EMBO Journal, 2016
    Co-Authors: Zhiyong Liu, Rongrong Lai, Si Liu, Wenlong Lin, Chuan Ouyang, He Huang, Xiaojian Wang
    Abstract:

    TANK‐binding kinase 1 (TBK1) activation is a central event in type I Interferon Production in anti‐virus innate immunity. However, the regulatory mechanism underlying TBK1 activation remains unclear. Here we report that Raf kinase inhibitory protein (RKIP) is essential for TBK1 activation and type I Interferon Production triggered by viral infection. Upon viral infection, RKIP is phosphorylated at serine 109 (S109) by TBK1. Phosphorylation of RKIP enhances its interaction with TBK1 and in turn promotes TBK1 autophosphorylation. Mutation of RKIP S109 to alanine abrogates the interaction between RKIP and TBK1, and the anti‐viral function of RKIP. RKIP deficiency inhibits intracellular double‐stranded RNA‐ or DNA‐induced type I Interferon Production. Consistently, RKIP deficiency renders the mice more susceptible to vesicular stomatitis virus (VSV) and herpes simplex virus (HSV) infections. This study reveals a previously unrecognized positive feedback loop between RKIP and TBK1 that is essential for type I Interferon Production in anti‐viral innate immunity. ![][1] TBK1 plays a central role in type I Interferon Production in innate immunity. Here we show that the TBK1–RKIP loop is important for TBK1 activation during anti‐viral innate immunity. Upon viral infection, TBK1 phosphorylates RKIP, which enhances its interaction with TBK1 and in turn promotes TBK1 autophosphorylation. [1]: /embed/graphic-1.gif