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NS1 influenza protein
The NS1 influenza protein (NS1) is a viral nonstructural protein encoded by the NS gene segments of type A, B and C influenza viruses. Also encoded by this segment is the nuclear export protein (NEP), formally referred to as NS2 protein, which mediates the export of influenza virus ribonucleoprotein (RNP) complexes from the nucleus, where they are assembled.〔(Influenza B and C Virus NEP (NS2) Proteins Possess Nuclear Export Activities ) Journal of Virology, August 2001, p. 7375-7383, Vol. 75, No. 16〕〔O'Neill RE, Talon J and Palese P (1998) The influenza virus NEP (NS2 protein) mediates the nuclear export of viral ribonucleoproteins. EMBO J, 17, 288–296.〕
==Characteristics==
The NS1 of influenza A virus is a 26,000 Dalton protein. It prevents polyadenylation of cellular mRNAs to circumvent antiviral responses of the host, e.g., maturation and translation of interferon mRNAs. NS1 might also inhibit splicing of pre-mRNA by binding to a stem-bulge region in U6 small nuclear RNA (snRNA).〔Lu, Y et al., 1995. Binding of the influenza virus NS1 protein to double-stranded RNA inhibits the activation of the protein kinase that phosphorylates the elF-2 translation initiation factor. Virology. 1995 Dec 1;214(1):222-8.〕 In addition, NS1 is probably able to suppress the interferon response in the virus-infected cell leading to unimpaired virus production.〔Kumar, KU, Srivastava, SP, Kaufma,n RJ. 1999. Double-stranded RNA-activated protein kinase (PKR) is negatively regulated by 60S ribosomal subunit protein L18. Mol Cell Biol. 1999 Feb;19(2):1116–25.〕
NS1 also binds dsRNA. Binding assays with NS1 protein mutants established that the RNA-binding domain of the NS1 protein is required for binding to dsRNA as well as for binding to polyA and U6 snRNA. In addition, dsRNA competed with U6 snRNA for binding to the NS1 protein, a result consistent with both RNAs sharing the same binding site on the protein. As a consequence of its binding to dsRNA, the NS1 protein blocks the activation of the dsRNA-activated protein kinase (PKR) in vitro. This kinase phosphorylates the alpha subunit of eukaryotic translation initiation factor 2 (elF-2 alpha), leading to a decrease in the rate of initiation of translation.〔 In the absence of NS1, this pathway is inhibited during anti-viral response to halt all protein translation – thus stopping the synthesis of viral proteins; however, the influenza virus' NS1 protein is an agent that circumvents host defenses to allows viral gene transcription to occur.
The NS1 protein can be divided into an N terminal (RNA binding) domain and C terminal (effector domain). The RNA binding domain is able to target RIG-I, and therefore prevent the activation of induction of interferon responses. At the effector domain, it interacts and inhibits cleavage and polyadenylation specificity factor (CPSF30). CPSF30 is part of processing pathway for cellular mRNAs, and its inhibition leads to inability of the cellular mRNA to be exported outside the nucleus for translation, thereby hindering the ability of host cell to produce Interferon-stimulated genes.
抄文引用元・出典: フリー百科事典『 ウィキペディア（Wikipedia）』
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