Herpes Simplex Virus is Akt-ing in translational control.
All viruses depend on the cellular protein synthesis machinery for the production of viral proteins. Thus, viruses have evolved a variety of strategies to avoid innate host responses that inhibit protein synthesis. In this issue of Genes & Development, Chuluunbaatar and colleagues (pp. 2627-2639) demonstrate that Herpes Simplex Virus-1 counteracts this response through viral kinase Us3, which mimics cellular kinase Akt to phosphorylate and repress tuberous sclerosis complex 2 (TSC2), resulting in the activation of mammalian target of rapamycin complex 1 (mTORC1) and enhancement of mRNA translation.
Department of Microbiology and Immunology, Stanford University School of Medicine, California 94305, USA.
Kara L
KL
Norman
Peter
P
Sarnow
D000818:Animals; D015967:Gene Expression Regulation, Viral; D018259:Herpesvirus 1, Human / Q000378:metabolism*; D006801:Humans; D010766:Phosphorylation; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism*; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D015398:Signal Transduction; D058570:TOR Serine-Threonine Kinases / Q000378:metabolism; D000077005:Tuberous Sclerosis Complex 2 Protein; D025521:Tumor Suppressor Proteins / Q000378:metabolism; D014764:Viral Proteins / Q000378:metabolism*
C000624653:TSC2 protein, human; D000077005:Tuberous Sclerosis Complex 2 Protein; D025521:Tumor Suppressor Proteins; D014764:Viral Proteins; D017346:Protein Serine-Threonine Kinases; D051057:Proto-Oncogene Proteins c-akt; D058570:TOR Serine-Threonine Kinases; C095207:US3 protein, Human herpesvirus 1