Cells have evolved a number of mechanisms to respond to stresses such as infections. These stress responses inhibit translation, which results in the aggregation of mRNAs and binding proteins in membraneless compartments called stress granules (SGs). SGs are important for organising cellular content, capturing mRNAs and proteins, and signalling cascades. Recent studies also suggest that SGs play a role in antiviral defence. Previous work by the lab of Nicolas Locker showed that feline calicivirus (FCV) prevents SG formation by cleaving the scaffolding protein G3BP1. Interestingly, they also observed that uninfected bystander cells contained G3BP1 foci. In this study (Iadevaia et al., 2022), they investigate a paracrine response triggered by infection and show that virus-free supernatant (VFS) from infected cells can induce SG-like formations in uninfected cells, which they term paracrine granules (PGs). Whilst PGs share some characteristics with SGs, they differ in size, abundance, RNA and protein composition, and disassembly dynamics. PGs were insensitive to cycloheximide treatment, and their formation was not found to be dependent on G3BP1. Furthermore, cells treated with VFS and then infected with FCV showed reduced viral replication, suggesting that PGs could be involved in antiviral activity. Although the origin of the paracrine messenger remains unknown, this study furthers our understanding of membraneless compartments in response to infection, and their role in mediating viral replication.
Viral infection can induce novel stress granule-like structures in bystander cells
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Viral infection can induce novel stress granule-like structures in bystander cells. J Cell Sci 15 February 2022; 135 (4): e135_e0403. doi:
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