Second-Site Mutation Outside of the U(S)10-12 Domain of Δγ(1)34.5 Herpes Simplex Virus 1 Recombinant Blocks the Shutoff of Protein Synthesis Induced by Activated Protein Kinase R and Partially Restores Neurovirulence

Eitemau Tebyg

• The Second-Site Mutation in the Herpes Simplex Virus Recombinants Lacking the γ(1)34.5 Genes Precludes Shutoff of Protein Synthesis by Blocking the Phosphorylation of eIF-2α
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• Chimeric HCMV/HSV-1 and Δγ(1)34.5 oncolytic herpes simplex virus elicit immune mediated antigliomal effect and antitumor memory()()
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• Preclinical Evaluation of Oncolytic Δγ (1)34.5 Herpes Simplex Virus Expressing Interleukin-12 for Therapy of Breast Cancer Brain Metastases
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• The γ(1)34.5 protein of herpes simplex virus 1 complexes with protein phosphatase 1α to dephosphorylate the α subunit of the eukaryotic translation initiation factor 2 and preclude the shutoff of protein synthesis by double-stranded RNA-activated protein kinase
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• Activated MEK Suppresses Activation of PKR and Enables Efficient Replication and In Vivo Oncolysis by Δγ(1)34.5 Mutants of Herpes Simplex Virus 1
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