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.