Caister Academic Press

Modulation of the Antiviral Response by Dengue Virus

Jorge L. Muñoz-Jordán and Irene Bosch
from: Frontiers in Dengue Virus Research (Edited by: Kathryn A. Hanley and Scott C. Weaver). Caister Academic Press, U.K. (2010)

Abstract

Dengue virus (DENV) produces a wide range of human illness, ranging from asymptomatic infections to hemorrhagic and potentially fatal disease. Severe disease is associated with high viremia, immune enhancement of sequential infections, and exacerbated inflammatory response. DENV is sensed in mammalian cells by endosomal and cytoplasmic receptors and stimulates the type-1 interferon (IFNα/ β) response. Secreted IFNα/ β stimulates JAK/STAT signaling, which results in the activation of IFNα/ β- stimulated genes that lead the infected cells toward the establishment of an antiviral response. Genomic technology has enabled the identification of a remarkable list of genes induced in human host cells in response to DENV infection. The results define antiviral and pro-inflammatory responses mainly composed of IFNα/ β- induced genes, which likely participate in the regulation of the immune response and vascular leakage during acute illness. DENV counteracts the IFNα/ β response of the host. The evidence indicates that non-structural proteins of DENV weaken IFNα/ β signaling, causing reduced activation of IFNα/ β-induced genes. The increased virus uptake, weakened host cell defense, and unrestrained inflammatory response likely predispose patients to develop severe illness. The unveiling of these virus-host interactions leads to a better understanding of dengue pathogenesis, and to innovative diagnostic and therapeutic approaches read more ...
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