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1 September 2006

Volume 194, Number 5
The Journal of Infectious Diseases 2006;194:600–607
© 2006 by the Infectious Diseases Society of America. All rights reserved.
0022-1899/2006/19405-0011$15.00
DOI: 10.1086/506451
MAJOR ARTICLE

Cellular Immune Activation in Children with Acute Dengue Virus Infections Is Modulated by Apoptosis

Khin S. Myint,1

Timothy P. Endy,1,a

Duangrat Mongkolsirichaikul,1

Choompun Manomuth,1

Siripen Kalayanarooj,2

David W. Vaughn,3,a

Ananda Nisalak,1

Sharone Green,4

Alan L. Rothman,4

Francis A. Ennis,4 and

Daniel H. Libraty4

1Department of Virology, Armed Forces Research Institute of Medical Sciences, and 2Department of Pediatrics, Queen Sirikit National Institute of Child Health, Bangkok, Thailand; 3Department of Virus Diseases, Walter Reed Army Institute of Research, Silver Spring, Maryland; 4Center for Infectious Disease and Vaccine Research, University of Massachusetts Medical School, Worcester, Massachusetts

Apoptosis is an important modulator of cellular immune responses during systemic viral infections. Peripheral‐blood mononuclear cell (PBMC) apoptosis and plasma soluble levels of CD95, a mediator of apoptosis, were determined in sequential samples from children participating in a prospective study of dengue virus (DV) infections. During the period of defervescence, levels of PBMC apoptosis were higher in children developing dengue hemorrhagic fever (DHF), the most severe form of illness, than in those with dengue fever (DF) and other, nondengue, febrile illnesses. CD8+ T lymphocytes made up approximately half of the peak circulating apoptotic PBMCs in DHF and DF. Maximum plasma levels of soluble CD95 were also higher in children with DHF than in those with DF. The level of PBMC apoptosis correlated with dengue disease severity. Apoptosis appears to be involved in modulation of the innate and adaptive immune responses to DV infection and is likely involved in the evolution of immune responses in other viral hemorrhagic fevers.

Received 11 January 2006; accepted 24 April 2006; electronically published 31 July 2006.

Reprints or correspondence: Dr. Daniel H. Libraty, Center for Infectious Disease and Vaccine Research, University of Massachusetts Medical School, Rm. S5‐326, 55 Lake Ave. N, Worcester, MA 01655 ().

Cited by

Atanu Basu, Umesh C. Chaturvedi. (2008) Vascular endothelium: the battlefield of dengue viruses. FEMS Immunology & Medical Microbiology 0:0, 080603023556983-???
Online publication date: 3-Jul-2008.
CrossRef
Sonia Melino, Maurizio Paci. (2007) Progress for dengue virus diseases. . FEBS Journal 274:12, 2986-3002
Online publication date: 1-Jul-2007.
CrossRef
Cameron P. Simmons, Stephen Popper, Christiane Dolocek, Tran Nguyen Bich Chau, Michael Griffiths, Nguyen Thi Phuong Dung, Truong Hoang Long, Dang Minh Hoang, Nguyen Vinh Chau, Le Thi Thu Thao, Tran Tinh Hien, David A. Relman, and Jeremy Farrar. (2007) Patterns of Host Genome–Wide Gene Transcript Abundance in the Peripheral Blood of Patients with Acute Dengue Hemorrhagic Fever. The Journal of Infectious Diseases 195:8, 1097-1107
Online publication date: 15-Apr-2007.
Abstract-Full Text-PDF Version (904 kB)

  • Potential conflicts of interest: none reported.

    Financial support: National Institutes of Health (grant NIH‐P01AI34533); US Army Medical Research and Materiel Command.

    The contents of this article are solely the responsibility of the authors and do not necessarily represent the official views of the National Institutes of Health or the Department of Defense.

  • Present affiliations: Division of Communicable Diseases and Immunology, Walter Reed Army Institute of Research, Silver Spring, Maryland (T.P.E.); Military Infectious Diseases Research Program, US Army Medical Research and Materiel Command, Fort Detrick, Maryland (D.W.V.).

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