While DCs also support EBOV replication, they remain in a state of paralysis depicted by in vitro studies where suppression of surface expressed maturation markers such as CD80, CD86, and MHC class II molecules post-infection have been observed paralleled with the upregulation of T cell inhibitory molecules such as B7-H1 resulting in PD1 mediated T cell apoptosis (25–27). Here, CD80 is linked to infection.