Transactivation of the Rous sarcoma virus long terminal repeat promoter by Marek's disease virus.

Transient expression of chloramphenicol acetyltransferase (CAT) was used to study Marek's diseases virus (MDV)-mediated transactivation of the Rous sarcoma virus long terminal repeat (RSV-LTR) promoter. Cotransfection experiments in primary avian cells were conducted using MDV high-molecular-weight DNA and plasmid pRSVcat. Increased CAT activity, relative to controls, was consistently observed in the presence of MDV. Enhanced CAT activity, expressed via the RSV-LTR promoter, was strictly dependent on the presence of MDV DNA or virus, suggesting that activation of the RSV-LTR promoter was due to factors expressed in MDV-infected cells. Differences in transactivation efficiency were observed between various strains and the serotypes of MDV. In particular, high- and low-passage pairs of serotype 1 MDV showed marked differences in their ability to increase CAT activity in pRSVcat-transfected cells. Attenuation of viral pathogenicity and decreased expression of some cell surface glycoproteins occur in high-passage MDV strains. Decreased transactivation ability in these same strains suggests that continuous passage in culture and attenuation may perturb a regulatory mechanism operating by transcriptional control. In addition, transactivation of the RSV-LTR promoter suggests that increased incidence of avian leukosis following vaccination by MDV may be due to MDV-mediated transactivation of endogenous ALV proviral LTR promoters. MDV-mediated transactivation was not limited to the RSV-LTR promoter. Serotype 3 MDV (HVT) efficiently transactivated the herpes simplex virus (HSV) alpha 4 (ICP4) and beta-TK promoters as well as the human cytomegalovirus (hCMV) immediate early promoter.