有哪些信誉好的足球投注网站the anti-interferon activity of conserved viral dutpase orf54 is essential for an effective mhv-68 infection守恒的病毒的anti-interferon活动dutpase orf54是必不可少的一个有效的mhv - 68感染.pdfVIP
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the anti-interferon activity of conserved viral dutpase orf54 is essential for an effective mhv-68 infection守恒的病毒的anti-interferon活动dutpase orf54是必不可少的一个有效的mhv - 68感染
The Anti-interferon Activity of Conserved Viral dUTPase ORF54 is Essential for an Effective MHV-68 Infection 1 2 2¤ 2 2 Ronika Sitapara Leang , Ting-Ting Wu , Seungmin Hwang , Lidia T. Liang , Leming Tong , Jennifer T. Truong2, Ren Sun1,2* 1 Molecular Biology Institute, University of California Los Angeles, Los Angeles, California, United States of America, 2 Department of Molecular and Medical Pharmacology, University of California Los Angeles, Los Angeles, California, United States of America Abstract Gammaherpesviruses such as KSHV and EBV establish lifelong persistent infections through latency in lymphocytes. These viruses have evolved several strategies to counteract the various components of the innate and adaptive immune systems. We conducted an unbiased screen using the genetically and biologically related virus, MHV-68, to find viral ORFs involved in the inhibition of type I interferon signaling and identified a conserved viral dUTPase, ORF54. Here we define the contribution of ORF54 in type I interferon inhibition by ectopic expression and through the use of genetically modified MHV-68. ORF54 and an ORF54 lacking dUTPase enzymatic activity efficiently inhibit type I interferon signaling by inducing the degradation of the type I interferon receptor protein IFNAR1. Subsequently, we show in vitro that the lack of ORF54 causes a reduction in lytic replication in the presence of type I interferon signaling. Investigation of the physiological consequence of IFNAR1 degradation and importance of ORF54 during MHV-68 in vivo infection demonstrates that ORF54 has an even greater impact on persistent infection than on lytic replication. MHV-68 lacking ORF5
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