¹IBMP-CNRS, rue du Général Zimmer, Strasbourg, France

Correspondence: Dr O Voinnet and Dr S Pfeffer, Institut de Biologie Moléculaire des Plantes, CNRS UPR-2357, 12, rue du Général Zimmer, 67084 Strasbourg Cedex, France. E-mail: sebastien.pfeffer@ibmp-ulp.u-strasbg.fr, olivier.voinnet@ibmp-ulp.u-strasbg.fr

Abstract

Viruses represent one of the main factors that cause normal cells to proliferate and to become malignant: up to 15% of all human cancers are associated with single or multiple virus infections, and several viruses have been recognized as causal agents of specific types of cancer. Viruses have evolved many strategies to prevent infected cells from becoming apoptotic and to evade the innate and adaptive immune responses of their hosts. The recent discovery that Epstein–Barr virus and other herpesviruses produce their own sets of micro (mi)RNAs brings an additional layer of complexity in this ongoing host–virus arms race and changes our initial views of the antiviral roles of RNA silencing in plants and insects. It seems that, rather than being inhibited by this process, many mammalian viruses can usurp or divert the host RNA silencing machinery to their advantage. Viral-encoded miRNAs can act both in cis, to ensure accurate expression of viral genomes, and in trans, to modify the expression of host transcripts. Here, we review the current knowledge on viral miRNAs and discuss how mammalian viruses can also perturb host miRNA expression. Those recent findings provide new insights into the role of viruses and miRNAs in cancer development.