Abstract

Dengue is a neglected disease caused by the infection of dengue virus which is transmitted by Aedes mosquitoes and to some, it could be fatal. Regardless of the enormous work devoted to research for the treatment of dengue, to this day there is no cure, and treatment is solely limited to supportive care by treating the symptoms. The inhibition of the viral RNA non-structural enzymes has been the most popular approach amongst the strategies applied to the search and development of dengue antivirals. This review is a compact digest of what is already known of the roles and the prospects of the dengue virus non-structural proteins NS1, NS2BNS3, NS4A, NS4B and NS5 as the targets for antiviral studies including the recent progress that has been published regarding their roles.

Highlights

  • The Dengue Virus (DENV) is an arthropodborne virus of the Flaviviridae genus which includes over 70 other important human pathogens such as Yellow Tick-Borne Encephalitis Virus (TBEV) [1]

  • Infection of this virus across different serotypes causes a range of illness extending from unapparent febrile illness, which often is diagnosed as Dengue Fever (DF) to an acute and potentially lethal hemorrhagic fever known as Dengue Hemorrhagic Fever (DHF) [3]

  • The ATPase/helicase and nucleoside triphosphatase (NTPase) activities of DENV NS3 share the same active site and both C-terminal domain activities combined are required for melting secondary structures prior to initiation of RNA synthesis and for the unwinding of RNA duplexes, either to separate double-stranded RNA intermediates formed during viral RNA synthesis or as a translocase that can remove proteins bound to viral RNA [27,28,29]

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Summary

Introduction

The Dengue Virus (DENV) is an arthropodborne virus (arbovirus) of the Flaviviridae genus which includes over 70 other important human pathogens such as Yellow Tick-Borne Encephalitis Virus (TBEV) [1]. Anti-viral approaches have explored structural and nonstructural proteins of DENV as targets. Laboratory; significantly reduced viral replication in DENV-2 infected Vero cells

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