Abstract
Dengue, the most prevalent arthropod-borne viral disease, is caused by the dengue virus (DENV), a member of the Flaviviridae family, and is a considerable public health threat in over 100 countries, with 2.5 billion people living in high-risk areas. However, no specific antiviral drug or licensed vaccine currently targets DENV infection. The replicon system has all the factors needed for viral replication in cells. Since the development of replicon systems, transient and stable reporter replicons, as well as reporter viruses, have been used in the study of various virological aspects of DENV and in the identification of DENV inhibitors. In this review, we summarize the DENV reporter replicon system and its applications in high-throughput screening (HTS) for identification of anti-DENV inhibitors. We also describe the use of this system in elucidation of the mechanisms of virus replication and viral dynamics in vivo and in vitro.
Highlights
IntroductionDengue virus (DENV), which includes four serotypes (DENV1–4), is transmitted to humans by Aedes mosquitos and is the etiological agent of dengue fever and dengue hemorrhagic fever [1]
Dengue virus (DENV), which includes four serotypes (DENV1–4), is transmitted to humans by Aedes mosquitos and is the etiological agent of dengue fever and dengue hemorrhagic fever [1].DENV causes an estimated 50–100 million cases of dengue fever, 500,000 cases of severe dengue (dengue hemorrhagic fever/dengue shock syndrome (DHF/DSS)), and more than 20,000 deaths each year in tropical and subtropical regions, representing a considerable public health threat in over 100 countries worldwide [2]
We describe a replication-competent DENV subgenomic and full-length replicon system composed of reporter genes
Summary
Dengue virus (DENV), which includes four serotypes (DENV1–4), is transmitted to humans by Aedes mosquitos and is the etiological agent of dengue fever and dengue hemorrhagic fever [1]. The DENV genome consists of approximately 11 kb, containing one large open-reading frame (ORF) This viral RNA encodes a polyprotein that is processed by cellular and viral proteases into three structural proteins (capsid (C), pre-membrane (prM), and envelope (E)), which form the virus particle, and seven nonstructural (NS) proteins (NS1: essential for RNA replication, NS2A: inhibition of interferon signal, NS2B: cofactor of NS3 protease, NS3: protease and helicase activity, NS4A: induction of membrane rearrangements, NS4B: inhibition of interferon signal, and NS5: methyltransferase and RNA polymerase activity, inhibition of interferon signal).
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