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Encephalomyocarditis virus protein 2B* antagonises innate immune signalling by interacting with 14-3-3 protein family members_C4PR_LIV

ABSTRACT: Encephalomyocarditis virus (EMCV) has for decades served as an important model RNA virus. Although most of the EMCV proteins are obtained via proteolytic cleavage of a long polyprotein, 2B* is expressed from a short overlapping open reading frame via an unusual protein-stimulated temporally dependent ribosomal frameshifting mechanism. The function of 2B* has not yet been characterised, though mutant viruses that are unable to express 2B* have a small plaque phenotype. Here we show that 2B* binds all seven members of the 14-3-3 protein family during virus infection. Binding is dependent on the 2B* C-terminal sequence RRNSS. IFN-β and IL-6 signalling are impeded following overexpression of 2B* but not a truncated version lacking the RRNSS residues, thus suggesting a 14-3-3-dependent role for 2B* in inhibiting MAVS signalling. We also find that this function is distinct from the effect of 2B* on plaque size, as a virus in which 2B* was similarly truncated exhibited near-wildtype plaque size, thus indicating that 2B* also harbours additional functions. This work provides the first identification of a role of 2B* in innate immune antagonism and expands our knowledge of the protein complement of this important model virus.

INSTRUMENT(S):

ORGANISM(S): Mesocricetus Auratus (golden Hamster)

TISSUE(S): Permanent Cell Line Cell, Cell Culture

SUBMITTER: Ed Emmott

LAB HEAD: Edward Emmott

PROVIDER: PXD062303 | Pride | 2025-08-12

REPOSITORIES: Pride

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			Action	DRS
	2Bstar_20210512.fasta	Fasta
	EE210508_Col_Sam2Bstar_Unfr.raw	Raw
	GoldenHamster_uniprot-proteome_UP000189706_31691prot_dl20210512.fasta	Fasta
	Sam_2021_2Bstar.zip	Other
	checksum.txt	Txt

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