FIG. 5.

In hepatic cells, virulent LCMV down-regulates PRH (A) and up-regulates VEGF (B). (A) Cells were infected with virulent or nonvirulent LCMV, and Western blot analyses of the cell lysates were done as described in Materials and Methods. Blots were probed with a rabbit anti-PRH antibody or an anti-β-actin antibody and were revealed by enhanced chemiluminescence. The relative amounts of PRH protein are shown above the Western blot, with the amount of uninfected hepatic cells grown for 72 h set to 1.0. (B) Infected monkey liver sections were subjected to immunohistochemistry to detect the expression of VEGF, which is controlled at the level of translation by eIF4E (30). The liver section on the left expressed little VEGF and was from a monkey infected with LCMV-ARM, whereas the section on the right expressed higher steady-state levels of VEGF and was from a monkey with LCMV-WE-mediated disease. Real-time quantitative PCRs of liver mRNAs from these monkey tissues revealed a three- to sevenfold increase in VEGF mRNA in diseased tissue.