Inhibition of host poly(A)-binding protein by virus (kw:KW-1101)

Poly(A) binding protein (PABPC1) normally stimulates mRNA translation by interacting with several translation initiation factors bound to the 5'- end of mRNAs. The interaction between PABPC1 and eIF4G forms a protein bridge between 5'- and 3'-ends, enhancing cap binding by eIF4E and RNA binding by eIF4G and PABPC1.

Numerous viruses interfere with PABPC1 function in translation initiation. Inhibiting host translation eventually leads to shutoff of host proteins expression and gives viruses transcripts a competitive edge for access to the cellular translation machinery. Preventing the expression of host proteins is also a strategy to counteract the antiviral response.
Viral inhibition can be achieved either by cleaving PABPC1 with virally encoded proteases, evicting it from translation initiation complexes or relocalizing it to the nucleus .

Viruses inhibiting PABPC1:

Family	Virus	Viral protein	PABPC1 inhibition strategy	references
Retroviridae	HIV-1	Protease	PABPC1 cleavage
Picornaviridae	Poliovirus	Protease 3C	PABPC1 cleavage
	Hepatitis A virus	Protease 3C	PABPC1 cleavage
	coxsackie virus	Protease 2A, protease 3C	PABPC1 cleavage
	Foot-and-mouth disease virus	?Leader protease	PABPC1 cleavage
Caliciviridae	MD145-12	Protease 3C	PABPC1 cleavage
	feline calicivirus	Protease 3C	PABPC1 cleavage
Reoviridae	Rotavirus	NSP3	Interacts with EIF4G and evicts PABC1 from initiation complexes. Nuclear relocalization of PABC1
Bunyaviridae	Bunyamwera virus	Nucleoprotein	Nuclear relocalization of PABC1
Togaviridae	Rubella virus	Capsid protein	PABC1 sequestration