Inhibition of host poly(A)-binding protein by virus

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