Dex-mediated diminishment of basal and MARV-induced expression of pro-inflammatory TNF (presumably with concomitant dysregulated signaling and immunocellular functioning), and reduced support from infiltrating immune cells depleted from circulation, liver and secondary lymphoid tissues, all likely contribute toward increased hepatocyte infection, foci generation, heightened virus shedding and potentially fatal tissue damage reminiscent of MVD in primates (e.g., massive hepatic necrosis and hemorrhage). Here, TNF is linked to infection.