PubMed Journals: J Virol

  Source:		PMID: 15919935
  Download:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1143636/pdf/2005-04.pdf

    		J Virol. 2005 Jun;79(12):7819-26.
			Cytokine responses in
			severe acute respiratory syndrome
			coronavirus-infected macrophages in vitro:
			possible relevance to pathogenesis.

			Cheung CY(1), Poon LL, Ng IH, Luk W, Sia
			SF, Wu MH, Chan KH, Yuen KY, Gordon S, Guan
			Y, Peiris JS.

			Author Information
			(1) Department of Microbiology, University
			Pathology Building, Queen Mary Hospital,
			Pokfulam Road, Hong Kong, Special Administrative
			Region, People's Republic of China.

			The pathogenesis of severe acute respiratory syndrome
			(SARS) remains unclear. Macrophages
			are key sentinel cells in the respiratory
			system, and it is therefore relevant to
			compare the responses of human macrophages
			to infections with the SARS coronavirus
			(SARS-CoV) and other respiratory viruses.
			Primary human monocyte-derived macrophages
			were infected with SARS-CoV in vitro. Virus
			replication was monitored by measuring the
			levels of positive- and negative-strand
			RNA, by immunofluorescence detection of
			the SARS-CoV nucleoprotein, and by titration
			of the infectious virus. The gene expression
			profiles of macrophages infected with SARS-CoV,
			human coronavirus 229E, and influenza A
			(H1N1) virus were compared by using microarrays
			and real-time quantitative reverse transcriptase
			PCR. Secreted cytokines were measured with
			an enzyme-linked immunosorbent assay. SARS-CoV
			initiated viral gene transcription and protein synthesis
			in macrophages, but replication was abortive
			and no infectious virus was produced. In
			contrast to the case with human coronavirus
			229E and influenza A virus, there was little
			or no induction of beta interferon (IFN-beta)
			in SARS-CoV-infected macrophages. Furthermore,
			SARS-CoV induced the expression of chemokines
			such as CXCL10/IFN-gamma-inducible
			protein 10 and CCL2/monocyte chemotactic
			protein 1. The poor induction of IFN-beta,
			a key component of innate immunity, and
			the ability of the virus to induce chemokines
			could explain aspects of the pathogenesis
			of SARS.

			DOI: 10.1128/JVI.79.12.7819-7826.2005
			PMCID: PMC1143636 PMID: 15919935 [Indexed
			for MEDLINE]

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