Target intelligence / Profile preview

Coxsackievirus A10 replicon (CV-A10 replicon)

Target
CV-A10 replicon
Molecular classification
Viral replication system, Subgenomic RNA construct, Genetic tool
01

Overview

The Coxsackievirus A10 (CV-A10) replicon is a laboratory-engineered subgenomic RNA molecule used as a research tool to study the replication of CV-A10, a significant pathogen in the Enterovirus C genus responsible for hand, foot, and mouth disease (HFMD) (Source: PubMed, PMID: 31433934). The replicon is typically constructed by replacing the structural P1 gene region with a reporter gene, such as luciferase, while retaining the non-structural protein-coding regions (P2 and P3) necessary for RNA replication (Source: Viruses, 2020). This modification allows the replicon to replicate its genome and express viral proteins within a host cell without producing infectious progeny, providing a safer and more efficient platform for high-throughput antiviral screening (Source: Antiviral Research, 2018). The primary therapeutic targets expressed by the replicon include the 3C protease (3Cpro), which is essential for polyprotein processing, and the 3D RNA-dependent RNA polymerase (3Dpol), which is responsible for genome synthesis (Source: Journal of Virology). Drugs like Rupintrivir target the 3Cpro expressed by the replicon to block viral replication, making the replicon system an invaluable asset for identifying and characterizing novel small-molecule inhibitors (Source: NIH/NCBI).

Other names
CVA10 repliconCoxsackievirus A10 subgenomic repliconCV-A10 reporter replicon
02

Mechanism of action

Inhibition of viral 3C protease (3Cpro) to prevent polyprotein cleavage, or inhibition of the 3D RNA-dependent RNA polymerase (3Dpol) to terminate viral RNA synthesis.

03

Biological functions

Viral RNA replicationViral protein translationPolyprotein processingReporter gene expression
04

Disease associations

Hand, foot, and mouth disease (HFMD)HerpanginaAseptic meningitisInfection
05

Safety considerations

Rapid development of viral resistance mutationsPotential off-target inhibition of host cellular proteasesCytotoxicity of nucleoside analogs in host cellsLimited translatability of replicon-based results to clinical infectious models
06

Interacting drugs

Rupintrivir

3 more in the full profile.

07

Biomarkers

Luciferase activityGreen fluorescent protein (GFP) expressionViral RNA copy number3C protease activity levels

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