Human TLR3 Recognizes Dengue Virus and Modulates Viral Replication In Vitro
Date Issued
2008
Date
2008
Author(s)
Tsai, Yi-Ting
Abstract
Dengue virus (DENV) causes dengue fever (DF) as well as dengue hemorrhagic fever (DHF)/ dengue shock syndrome (DSS) that occur in more than 100 countries and usually in the tropical and subtropical regions of the world. A clearer understanding of its host-virus interaction is imperative for prophylaxis and treatment of this disease. Aberrant cytokine overproduction in host after DENV infection has been established as the cause of DHF. However, the innate immune recognition of DENV and inflammatory response elicited at the initial stages of infection have not been well elucidated. The aim of this study was to clarify the interaction between DENV and human toll-like receptors, which comprise the first line of innate immunity by activating local or systemic inflammatory response. This study found that endosomal acidification is required for DENV-2 to activate the human monocytic cell THP-1. Using the HEK293-TLR expression system and RNAi-based knockdown techniques, the experiments demonstrated that DENV-2 can be recognized mainly by TLR3, but not by the plasma membrane-anchored TLR. Further, TLR3-mediated IFN response has strong potential for inhibiting virus replication and significantly diminishes the in vitro cytopathic effect (CPE) of DENV-2, thus promoting cell survival. The findings of this study illustrate the in vitro interaction between DENV-2 and different TLR molecules which elucidate host-virus interaction and may enhance understanding of viral pathogenesis.
Subjects
Monocytes
Macrophages
Viral
Cytokines
Chemokines
Cell Activation
SDGs
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