PubMed Journals: Proc Natl Acad Sci U S A

  Source:		PMID: 16912115
  Download:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1568942/pdf/zpq12885.pdf

    		Proc Natl Acad Sci U S A. 2006 Aug
     		22;103(34):12885-90. Epub 2006 Aug 15.

			Severe acute respiratory syndrome coronavirus
			nsp1 protein suppresses host gene expression by
			promoting host mRNA degradation.

			Kamitani W(1), Narayanan K, Huang C, Lokugamage
			K, Ikegami T, Ito N, Kubo H, Makino S.

			Author Information
			(1) Department of Microbiology, University
			of Texas Medical Branch, Galveston, TX 77555-1019,

			Severe acute respiratory syndrome (SARS) coronavirus
			(SCoV) causes a recently emerged human disease
			associated with pneumonia. The 5' end two-thirds
			of the single-stranded positive-sense viral
			genomic RNA, gene 1, encodes 16 mature proteins.
			Expression of nsp1, the most N-terminal gene
			1 protein, prevented Sendai virus-induced
			endogenous IFN-beta mRNA accumulation without
			inhibiting dimerization of IFN regulatory factor 3,
			a protein that is essential for
			activation of the IFN-beta promoter. Furthermore,
			nsp1 expression promoted degradation of
			expressed RNA transcripts and host endogenous
			mRNAs, leading to a strong host protein synthesis
			inhibition. SCoV replication also promoted
			degradation of expressed RNA transcripts
			and host mRNAs, suggesting that nsp1 exerted
			its mRNA destabilization function in infected
			cells. In contrast to nsp1-induced mRNA
			destablization, no degradation of the 28S
			and 18S rRNAs occurred in either nsp1-expressing
			cells or SCoV-infected cells. These data
			suggested that, in infected cells, nsp1
			promotes host mRNA degradation and thereby
			suppresses host gene expression, including
			proteins involved in host innate immune
			functions. SCoV nsp1-mediated promotion
			of host mRNA degradation may play an important
			role in SCoV pathogenesis.

			DOI: 10.1073/pnas.0603144103 PMCID: PMC1568942
			PMID: 16912115 [Indexed for MEDLINE]

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