Marek's disease virus oncogenicity: Molecular mechanisms

This chapter discusses the oncogenicity of Marek's disease virus (MDV). It provides an overview of the roles of MDV genes that are potentially associated with latency/transformation. The onset of MDV-induced tumors is very rapid. The ability to induce rapid-onset tumors resembling those caused by some of the acutely transforming retroviruses suggests the direct involvement of virus-encoded transforming gene(s) in oncogenesis. Biochemical and genetic studies carried out in recent years suggest that Meq is the principal oncogene of MDV. Meq is a versatile protein that binds DNA, RNA, and a variety of other proteins. It also plays a potential role in the virulence replication and latency of MDV. Various investigations aimed at unravelling the oncogenic determinants of MDV have led to the identification of a number of other genes that have potential roles in the pathogenesis of MDV. Some of these MDV genes with a potential role in Marek's disease pathogenicity include the BamH1–H family of transcripts, the pp38/pp24 group of cytoplasmic phosphoproteins, the MDV-encoded CXC chemokine (vIL-8), the MDV-encoded telomerase RNA (vTR) subunit, and the MDV ICP4 homologue-related transcripts. The application of rapid, targeted, or random mutagenesis techniques enables rapid delineation of the molecular mechanisms and determinants for MDV-induced oncogenesis.