PubMed Journals: Virol J

  Source:		PMID: 16571117
  Download:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1444920/pdf/1743-422X-3-17.pdf

    		Virol J. 2006 Mar 29;3:17.
			Inhibition of cytokine gene expression and
			induction of chemokine genes in non-lymphatic
			cells infected with SARS coronavirus.

			Spiegel M(1), Weber F.

			Author Information
			(1) Abteilung Virologie, Institut für Medizinische
			Mikrobiologie und Hygiene, Universität,
			Freiburg, D-79008 Freiburg, Germany.

			BACKGROUND: SARS coronavirus (SARS-CoV)
			is the etiologic agent of the severe acute
			respiratory syndrome. SARS-CoV mainly infects
			tissues of non-lymphatic origin, and the
			cytokine profile of those cells can determine
			the course of disease. Here, we investigated
			the cytokine response of two human non-lymphatic
			cell lines, Caco-2 and HEK 293, which are
			fully permissive for SARS-CoV. RESULTS:
			A comparison with established cytokine-inducing
			viruses revealed that SARS-CoV only weakly
			triggered a cytokine response. In particular,
			SARS-CoV did not activate significant transcription
			of the interferons IFN-alpha, IFN-beta,
			IFN-lambda1, IFN-lambda2/3, as well as of
			the interferon-induced antiviral genes ISG56
			and MxA, the chemokine RANTES and the interleukine
			IL-6. Interestingly, however, SARS-CoV strongly
			induced the chemokines IP-10 and IL-8 in
			the colon carcinoma cell line Caco-2, but
			not in the embryonic kidney cell line 293.
			CONCLUSION: Our data indicate that SARS-CoV suppresses
			the antiviral cytokine system of non-immune
			cells to a large extent, thus buying time
			for dissemination in the host. However,
			synthesis of IP-10 and IL-8, which are established
			markers for acute-stage SARS, escapes the
			virus-induced silencing at least in some
			cell types. Therefore, the progressive infiltration
			of immune cells into the infected lungs
			observed in SARS patients could be due to
			the production of these chemokines by the
			infected tissue cells.

			DOI: 10.1186/1743-422X-3-17 PMCID: PMC1444920
			PMID: 16571117 [Indexed for MEDLINE]

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