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Journal of Virology, April 2001, p. 3501-3508, Vol. 75, No. 8
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.8.3501-3508.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Human Dendritic Cells Are Activated by Dengue Virus Infection: Enhancement by Gamma Interferon and Implications for Disease Pathogenesis

Daniel H. Libraty,1,2,* Sathit Pichyangkul,3 Chuanpis Ajariyakhajorn,2 Timothy P. Endy,2,4 and Francis A. Ennis1

Center for Infectious Disease and Vaccine Research, University of Massachusetts Medical School, Worcester, Massachusetts1; Department of Virology2 and Department of Immunology,3 Armed Forces Research Institute of Medical Sciences, Bangkok, Thailand; and Department of Virus Diseases, Walter Reed Army Institute of Research, Silver Spring, Maryland4

Received 28 August 2000/Accepted 8 January 2001

The ability of dendritic cells (DCs) to shape the adaptive immune response to viral infection is mediated largely by their maturation and activation state as determined by the surface expression of HLA molecules, costimulatory molecules, and cytokine production. Dengue is an emerging arboviral disease where the severity of illness is influenced by the adaptive immune response to the virus. In this report, we have demonstrated that dengue virus infects and replicates in immature human myeloid DCs. Exposure to live dengue virus led to maturation and activation of both the infected and surrounding, uninfected DCs and stimulated production of tumor necrosis factor alpha (TNF-alpha ) and alpha interferon (IFN-alpha ). Activation of the dengue virus-infected DCs was blunted compared to the surrounding, uninfected DCs, and dengue virus infection induced low-level release of interleukin-12 p70 (IL-12 p70), a key cytokine in the development of cell-mediated immunity (CMI). Upon the addition of IFN-gamma , there was enhanced activation of dengue virus-infected DCs and enhanced dengue virus-induced IL-12 p70 release. The data suggest a model whereby DCs are the early, primary target of dengue virus in natural infection and the vigor of CMI is modulated by the relative presence or absence of IFN-gamma in the microenvironment surrounding the virus-infected DCs. These findings are relevant to understanding the pathogenesis of dengue hemorrhagic fever and the design of new vaccination and therapeutic strategies.

* Corresponding author. Mailing address: USAMC-AFRIMS, Department of Virology, APO AP 96546. Phone: 66-2-644-4674. Fax: 66-2-644-4760. E-mail: dlibraty{at}mozart.inet.co.th or libratydh{at}thai.amedd.army.mil.

Journal of Virology, April 2001, p. 3501-3508, Vol. 75, No. 8
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.8.3501-3508.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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