Fine-tuning translation kinetics selection as the driving force of codon usage bias in the hepatitis A virus capsid.

ABSTRACT: Hepatitis A virus (HAV), the prototype of genus Hepatovirus, has several unique biological characteristics that distinguish it from other members of the Picornaviridae family. Among these, the need for an intact eIF4G factor for the initiation of translation results in an inability to shut down host protein synthesis by a mechanism similar to that of other picornaviruses. Consequently, HAV must inefficiently compete for the cellular translational machinery and this may explain its poor growth in cell culture. In this context of virus/cell competition, HAV has strategically adopted a naturally highly deoptimized codon usage with respect to that of its cellular host. With the aim to optimize its codon usage the virus was adapted to propagate in cells with impaired protein synthesis, in order

SUBMITTER: Aragones L 

PROVIDER: S-EPMC2832697 | biostudies-literature | 2010 Mar

REPOSITORIES: biostudies-literature