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Flavivirus replication refers to the process by which flaviviruses—enveloped, single-stranded positive-sense RNA viruses—copy their RNA and produce new virus particles in infected cells. Mediated by a coordinated action of viral nonstructural proteins (NS1, NS2a, NS2b, NS3, NS4a, NS4b, NS5) and select host factors and membranes, the process initiates when the virus enters the cell via receptor-mediated endocytosis and uncoats, releasing its RNA genome. The viral RNA is translated into a single polyprotein, which is processed primarily at the endoplasmic reticulum (ER), and viral nonstructural proteins anchor into the ER membrane, creating a membrane-associated replication complex. The complex replicates the viral RNA via a negative-strand RNA intermediate, packages progeny genomes into new nucleocapsids, and directs the assembly, maturation, and release of infectious virions. These steps collectively define flavivirus replication, which is essential for viral propagation, pathogenesis, and is a major focus of research for antiviral drug development.
Mechanisms are drug-specific and include: - Inhibition of RNA-dependent RNA polymerase (e.g., NS5 protein inhibitors) - Inhibition of viral protease (e.g., NS3 protease inhibitors) - Interference with host–virus protein interactions
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