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15 April 2007

Volume 195, Number 8
The Journal of Infectious Diseases 2007;195:1097–1107
© 2007 by the Infectious Diseases Society of America. All rights reserved.
0022-1899/2007/19508-0005$15.00
DOI: 10.1086/512162
MAJOR ARTICLE

Patterns of Host Genome–Wide Gene Transcript Abundance in the Peripheral Blood of Patients with Acute Dengue Hemorrhagic Fever

Cameron P. Simmons,1,a

Stephen Popper,3,a

Christiane Dolocek,1

Tran Nguyen Bich Chau,1

Michael Griffiths,3

Nguyen Thi Phuong Dung,1

Truong Hoang Long,1

Dang Minh Hoang,1

Nguyen Vinh Chau,2

Le Thi Thu Thao,2

Tran Tinh Hien,2

David A. Relman,3,4 and

Jeremy Farrar1

1Oxford University Clinical Research Unit, 2Hospital for Tropical Diseases, Ho Chi Minh City, Vietnam; 3Departments of Microbiology and Immunology and of Medicine, Stanford University, Stanford, and 4VA Palo Alto Health Care System, Palo Alto, California

Responses by peripheral blood leukocytes may contribute to the pathogenesis of dengue hemorrhagic fever (DHF). We used DNA microarrays to reveal transcriptional patterns in the blood of 14 adults with DHF. Acute DHF was defined by an abundance of transcripts from cell cycle– and endoplasmic reticulum (ER)–related genes, suggesting a proliferative response accompanied by ER stress. Transcript‐abundance levels for immunoresponse‐associated genes, including cell surface markers, immunoglobulin, and innate response elements, were also elevated. Twenty‐four genes were identified for which transcript abundance distinguished patients with dengue shock syndrome (DSS) from those without DSS. All the gene transcripts associated with DSS, many of which are induced by type I interferons, were less abundant in patients with DSS than in those without DSS. To our knowledge, these data provide the first snapshot of gene‐expression patterns in peripheral blood during acute dengue and suggest that DSS is associated with attenuation of selected aspects of the innate host response.

Received 31 August 2006; accepted 10 November 2006; electronically published 5 March 2007.

Reprints or correspondence: Dr. Cameron Simmons, Oxford University Clinical Research Unit, 190 Ben Ham Tu, Ho Chi Minh City District 5, Vietnam ().

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  • Potential conflicts of interest: none reported.

    Financial support: Wellcome Trust (to C.P.S. and J.F.); Horn Foundation (grant to D.A.R.).

  • Both authors contributed equally to this work.

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