Linking Kaposi virus to cancer-associated cytokines.
Viruses have evolved elaborate strategies to regulate host gene expression, thereby adapting to host stress responses against infection. In a recent report, it was shown that a human oncogenic herpesvirus, Kaposi sarcoma herpesvirus, activates the p38-MK2 pathway to stabilise cytokine transcripts. Specifically, a viral latent protein, kaposin B, binds to and activates MK2, leading to the stabilisation of AU-rich element (ARE)-containing mRNAs, which normally have only a short lifespan. Although the exact mechanism for p38-MK2 activation remains unclear, this study provides a new direction linking viral infection to selective mRNA turnover and cytokine biosynthesis.
Wang
Hsei-Wei
HW
Institute of Microbiology and Immunology, National Yang-Ming University, No. 155 Sec 2 Li-Nong Street, Taipei 112, Taiwan. hwwang@ym.edu.tw
Boshoff
Chris
C
D016207:Cytokines / Q000096:biosynthesis* / Q000235:genetics; D019288:Herpesvirus 8, Human / Q000378:metabolism / Q000502:physiology*; D006801:Humans; D020935:MAP Kinase Signaling System / Q000235:genetics*; D008954:Models, Biological; D009369:Neoplasms / Q000378:metabolism / Q000821:virology*; D012333:RNA, Messenger / Q000378:metabolism; D015854:Up-Regulation; D014764:Viral Proteins / Q000378:metabolism*; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism
D016207:Cytokines; D012333:RNA, Messenger; D014764:Viral Proteins; C120136:kaposin B protein, Human herpesvirus 8; D048051:p38 Mitogen-Activated Protein Kinases