Differential effects of ras and jun family members on complex retrovirus promoter activities

Abstract

Infection by complex retroviruses such as Visna-maedi, HIV1, HTLV-I and HFV is generally not followed by particle production, but rather by a more or less prolonged latency period. Knowledge of the mechanisms triggering an infectious cycle from the latent provirus(es) is of great importance in comprehending the appearance of the disease. It is currently admitted that cellular factors regulate viral expression. In this paper, we report the ability of ras, c-jun, jun-B and jun-D to diversely stimulate the LTR promoter activity of these retroviruses. Transient transfection assays using a luciferase reporter gene linked to LTR show that the Visna-maedi virus LTR, despite high intrinsic activity, is stimulated by Ha-ras and c-jun. The HTLV-I and HIV1 LTR were identically stimulated by ras, but differently by c-jun. In contrast, jun-B and jun-D were weaker activators, since they respectively stimulated only HTLV-I LTR and HIV1 LTR. HFV LTR remains unresponsive to either of these factors.