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. Author manuscript; available in PMC: 2011 Nov 17.
Published in final edited form as: Expert Rev Neurother. 2009 Apr;9(4):505–517. doi: 10.1586/ern.09.9

Figure 2. Nonessential viral proteins that are needed to counteract the dsRNA-dependent PKR pathway that is activated upon viral infection.

Figure 2

The schematic depicts the PKR pathway that is initiated following virus infection. Expression of PKR is activated by the interferon signaling pathway that is initiated upon viral infection. PKR activation (phosphorylation) is induced in response to dsRNA that is produced in virally infected cells. Active PKR phosphorylates eIF2α and thereby inhibits protein synthesis and blocks the production of viral proteins. PKR also activates the transcription factor NF-κB and induces an antiviral immune response. In order to counteract this pathway, γ34.5 retargets protein phosphatase-1α to induce dephosphorylation of eIF2α. US11 (if present with immediate-early gene kinetics) is able to inhibit PKR by a different mechanism, and the multifunctional ICP0 protein is also thought to play a role in inactivation of the interferon and PKR pathways. Activation of the Ras signaling pathway inhibits PKR activity and complements for the lack of γ34.5 (this example illustrates Ras activation after binding of EGF to its receptor).

HSV: Herpes simplex virus; NF: Nuclear factor; PKR: RNA-dependent protein kinase.