Rna-binding proteins at the host-pathogen interface targeting viral regulatory elements

Viral RNAs contain the information needed to synthesize their own proteins, to replicate, and to spread to susceptible cells. However, due to their reduced coding capacity RNA viruses rely on host cells to complete their multiplication cycle. This is largely achieved by the concerted action of regul...

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Detalhes bibliográficos
Autores: Embarc Buh, Azman, Francisco Velilla, María del Rosario, Martínez Salas, Encarnación
Formato: artículo
Fecha de publicación:2021
País:España
Recursos:Universidad Autónoma de Madrid
Repositorio:Biblos-e Archivo. Repositorio Institucional de la UAM
Idioma:inglés
OAI Identifier:oai:repositorio.uam.es:10486/718271
Acesso em linha:http://hdl.handle.net/10486/718271
https://dx.doi.org/10.3390/v13060952
Access Level:acceso abierto
Palavra-chave:RNA-binding proteins
RNA viruses
translation control
stress granules
trafficking factors
IRES elements
ER-Golgi
RNA methylation
Biología y Biomedicina / Biología
Descrição
Resumo:Viral RNAs contain the information needed to synthesize their own proteins, to replicate, and to spread to susceptible cells. However, due to their reduced coding capacity RNA viruses rely on host cells to complete their multiplication cycle. This is largely achieved by the concerted action of regulatory structural elements on viral RNAs and a subset of host proteins, whose dedicated function across all stages of the infection steps is critical to complete the viral cycle. Importantly, not only the RNA sequence but also the RNA architecture imposed by the presence of specific structural domains mediates the interaction with host RNA-binding proteins (RBPs), ultimately affecting virus multiplication and spreading. In marked difference with other biological systems, the genome of positive strand RNA viruses is also the mRNA. Here we focus on distinct types of positive strand RNA viruses that differ in the regulatory elements used to promote translation of the viral RNA, as well as in the mechanisms used to evade the series of events connected to antiviral response, including translation shutoff induced in infected cells, assembly of stress granules, and trafficking stress