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Abstract

RNA granules are dynamic cellular structures essential for proper gene expression and homeostasis. The two principal types of cytoplasmic RNA granules are stress granules, which contain stalled translation initiation complexes, and processing bodies (P bodies), which concentrate factors involved in mRNA degradation. RNA granules are associated with gene silencing of transcripts; thus, viruses repress RNA granule functions to favor replication. This article discusses the breadth of viral interactions with cytoplasmic RNA granules, focusing on mechanisms that modulate the functions of RNA granules and that typically promote viral replication. Currently, mechanisms for virus manipulation of RNA granules can be loosely grouped into three nonexclusive categories: () cleavage of key RNA granule factors, () regulation of PKR activation, and () co-opting of RNA granule factors for new roles in viral replication. Viral modulation of RNA granules supports productive infection by inhibiting their gene-silencing functions and counteracting their role in linking stress sensing with innate immune activation.

Keyword(s): G3BPP bodiesPKRstress granules

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Cytoplasmic RNA Granules and Viral Infection: Video 1
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/content/journals/10.1146/annurev-virology-031413-085505
2014-09-29
2025-04-27
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    Virus-induced stress granules () forming in cells infected with coxsackievirus B3 that produces dsRed fluorescent protein as a marker of robust replication. HEK cells are expressing Tia1-GFP () as a marker for stress granules, which translocates from the nucleus to cytoplasm as infection initiates. Expression of Tia1-GFP makes the cells more prone to stress granule formation, which generally delays or inhibits coxsackievirus B3 replication. In other infected cells, stress granules shrink or disperse after they appear, or they persist as residual pseudo–stress granules that no longer contain stalled translation complexes.

  • Article Type: Review Article
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