PubMed Journals: PLoS Pathog

  Source:		PMID: 17696609
  Download:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1941749/pdf/ppat.0030112.pdf

    		PLoS Pathog. 2007 Aug 10;3(8):e112.
			Functional genomics highlights differential
			induction of antiviral pathways in the lungs
			of SARS-CoV-infected macaques.

			de Lang A(1), Baas T, Teal T, Leijten LM,
			Rain B, Osterhaus AD, Haagmans BL, Katze

			Author Information
			(1) Department of Virology, Erasmus Medical Center,
			Rotterdam, The Netherlands.

			The pathogenesis of severe acute respiratory syndrome
			coronavirus (SARS-CoV) is likely mediated
			by disproportional immune responses and
			the ability of the virus to circumvent innate
			immunity. Using functional genomics, we
			analyzed early host responses to SARS-CoV
			infection in the lungs of adolescent cynomolgus
			macaques (Macaca fascicularis) that show
			lung pathology similar to that observed
			in human adults with SARS. Analysis of gene
			signatures revealed induction of a strong
			innate immune response characterized by
			the stimulation of various cytokine and
			chemokine genes, including interleukin (IL)-6,
			IL-8, and IP-10, which corresponds to the
			host response seen in acute respiratory distress
			syndrome. As opposed to many in vitro experiments,
			SARS-CoV induced a wide range of type I
			interferons (IFNs) and nuclear translocation
			of phosphorylated
			signal transducer and activator of transcription 1
			in the lungs of macaques. Using
			immunohistochemistry, we revealed that these
			antiviral signaling pathways were differentially
			regulated in distinctive subsets of cells.
			Our studies emphasize that the induction
			of early IFN signaling may be critical to
			confer protection against SARS-CoV infection
			and highlight the strength of combining
			functional genomics with immunohistochemistry
			to further unravel the pathogenesis of SARS.

			DOI: 10.1371/journal.ppat.0030112
			PMCID: PMC1941749 PMID: 17696609 [Indexed
			for MEDLINE]

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