However, inflammation [11, 12], hypoxia [13–15], oxidative stress [16] and co-infection with other viruses such as HIV-1[17–19] and other herpesviruses [20–22] have been shown, mostly in experimental settings, to trigger KSHV reactivation from latency through the release of inflammatory cytokines such as IFN-γ, hepatocyte growth factor/scatter factor and Oncostatin M [11, 12, 17, 23, 24] or the production of reactive oxygen species (ROS) [16, 25, 26]. Here, HGF is linked to coinfection.