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			PubMed Journals: Microbes Infect

  Source:		PMID: 15777647
  Download:	https://www.sciencedirect.com/science/article/pii/S1286457905000067

    		Microbes Infect. 2005 Feb;7(2):248-59. Epub
     		2005 Jan 22.

			Microarray and real-time RT-PCR analyses
			of differential human gene expression patterns
			induced by severe acute respiratory syndrome
			(SARS) coronavirus infection of Vero cells.

			Leong WF(1), Tan HC, Ooi EE, Koh DR, Chow
			VT.

			Author Information
			(1) Human Genome Laboratory, Department
			of Microbiology, Faculty of Medicine, National
			University of Singapore, Kent Ridge, Singapore
			117597, Singapore.

			Vero E6 African green monkey kidney cells
			are highly susceptible to infection with
			the newly emerging severe acute respiratory syndrome
			coronavirus (SARS-CoV), and they are permissive
			for rapid viral replication, with resultant
			cytopathic effects. We employed cDNA microarray
			analysis to characterize the cellular
			transcriptional responses of homologous
			human genes at 12 h post-infection. Seventy
			mRNA transcripts belonging to various functional
			classes exhibited significant alterations
			in gene expression. There was considerable
			induction of heat shock proteins that are
			crucial to the immune response mechanism.
			Modified levels of several transcripts involved
			in pro-inflammatory and anti-inflammatory
			processes exemplified the balance between
			opposing forces during SARS pathogenesis.
			Other genes displaying altered transcription
			included those associated with host translation,
			cellular metabolism, cell cycle, signal
			transduction, transcriptional regulation,
			protein trafficking, protein modulators,
			and cytoskeletal proteins. Alterations in
			the levels of several novel transcripts
			encoding hypothetical proteins and expressed
			sequence tags were also identified. In addition,
			transcription of apoptosis-related genes DENN and hIAP1
			was upregulated in contrast to FAIM. Elevated
			Mx1 expression signified a strong host response
			to mediate antiviral resistance. Also expressed
			in infected cells was the C-terminal alternative
			splice variant of the p53 tumor suppressor
			gene encoding a modified truncated protein
			that can influence the activity of wild-type
			p53. We observed the interplay between various
			mechanisms to favor virus multiplication
			before full-blown apoptosis and the triggering
			of several pathways in host cells in an
			attempt to eliminate the pathogen. Microarray
			analysis identifies the critical host-pathogen
			interactions during SARS-CoV infection and
			provides new insights into the pathophysiology of
			SARS.

			DOI: 10.1016/j.micinf.2004.11.004 PMID: 15777647
			[Indexed for MEDLINE]

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