Inhibition of PKR by vaccinia virus: role of the N- and C-terminal domains of E3L.

Article Details

Citation

Langland JO, Jacobs BL

Inhibition of PKR by vaccinia virus: role of the N- and C-terminal domains of E3L.

Virology. 2004 Jul 1;324(2):419-29.

PubMed ID
15207627 [ View in PubMed
]
Abstract

The process of eukaryotic translation initiation can be regulated by a highly conserved mechanism involving the phosphorylation of the translation initiation factor eIF2 on the alpha subunit. This mechanism is recognized as an efficient step in the host antiviral response. Vaccinia virus (VV), like many other viruses, encodes proteins to overcome this inhibitory process. The C-terminus of the vaccinia virus E3L is known to bind to double-stranded RNA (dsRNA) thereby sequestering the activator of this antiviral response. In this report, the N-terminus of E3L was found to be required for the additional regulation of eIF2alpha phosphorylation. This phosphorylation event did not lead to a global shutdown in protein synthesis. Because the N-terminus of E3L is required for full viral pathogenesis in mice, these results suggest an alternative role of eIF2alpha phosphorylation in regulating viral replication.

DrugBank Data that Cites this Article

Polypeptides
NameUniProt ID
Interferon-induced, double-stranded RNA-activated protein kinaseP19525Details