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Abstract
GETV infection triggers the formation of Nsp3-G3BP aggregates that differ from typical stress granules.
- Nsp3-G3BP aggregates formed during GETV infection rely on the activation of the PKR/eIF2α signaling pathway.
- The Nsp3 HVD domain inhibits stress granule formation by binding to the G3BP NTF2 domain.
- Knockout of G3BP in NCI-H1299 cells does not affect GETV replication.
- Overexpression of G3BP to create genuine stress granules significantly reduces GETV replication.
- These findings suggest a novel role for GETV Nsp3 in modifying stress granule composition and the cellular stress response.
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