From our results, it was clear that the mutation in VP24 was critical for pathogenicity since EBOV/Makona-rgMA-10979 behaved similarly to EBOV/Makona-rgMA, EBOV/Makona-MA-PP1, and EBOV/Mayinga-MA in terms of uncontrolled viral replication, increased release of pro-inflammatory cytokines and chemokines, lymphopenia, and the ability to cause severe disease and lethal infection in mice. This evidence concerns the gene RGMA and infection.