The kinetic expression analysis of the cluster mdv1- mir-M9-M4, genes meq and vIL-8 differs between the lytic and latent phases of Marek's disease virus infection

hal-00776065International audienceGallid herpesvirus 2 (GaHV-2 or MDV-1, for Marek's disease virus type one) is a lymphotropic alphaherpesvirus that causes malignant CD4+ T-cell lymphoma in chicken. The rapid onset of tumour development and high mortality rates of Marek's disease (MD) make it an ideal model for studies of the induction of lymphoma by a virus in its natural host (Osterrieder et al., 2006). Like other herpesviruses, GaHV-2 has a two-phase life cycle, consisting of a lytic and a latent phase, the latter closely associated with the oncogenesis of GaHV-2. The lymphomagenesis induced by GaHV-2 seems to be complex and multifactorial and the precise molecular mechanisms of cell transformation remain unclear. Several gene products, such as Meq, vTR, vIL-8 and mdv1-mir-M4-5P, have been implicated in the process of oncogenesis (Lupiani et al., 2004; Parcells et al., 2001; Trapp et al., 2006; Zhao et al., 2011). As other mardiviruses and simplexviruses, GaHV-2 has a type E genome consisting of one unique long (UL) and one unique short (US) region, encompassing core genes and flanked by the inverted internal and terminal repeats of the long regions (IRL/TRL) and short regions (IRS/TRS), respectively (Tulman et al., 2000). The herpesvirus genusspecific genes, particularly those implicated in pathogenesis in the specific host, are located principally in the TRL/IRL and IRS/TRS regions. Several of the proteins encoded by the 30 predicted ORFs in the IRL/TRL regions have been characterized: (i) the product of meq the major oncogene (Jones et al., 1992; Levy et al., 2003; Liu & Kung, 2000; Liu et al., 1998), (ii) vIL-8, a viral protein analogous to chicken IL-8 (Liu et al., 1999; Parcells et al., 2001; Peng et al., 1995), (iii) the proteins of the 14 kDa family, including 14 kDA, B and C (Bradley et al., 1989; Hong et al., 1995), (iv) the products of R-LORF5a and R-LORF4 (Jarosinski et al., 2005; Ohashi et al., 1994