In the study of immunological mechanisms of Ebola virus disease humans, we showed that fatal infection is associated with aberrant innate immunity and global suppression of adaptive immunity [, [9] [10] [11] [12] . The innate immune reaction is characterized by a 'cytokine storm', with a hyper secretion of numerous pro-inflammatory cytokines, chemokines and growth factors, and by the noteworthy absence of antiviral interferon (IFN)-α [9, 13, 14] . Immunosuppression of adaptive immunity is characterized by very low levels of circulating cytokines produced by T lymphocytes and by massive loss of peripheral CD4 and CD8 lymphocytes, probably through Fas/FasL-mediated apoptosis. Finally, we hypothesized that a viral protein with super-antigen activity might be involved in the massive T cell apoptosis [15] . In striking contrast with fatal outcome, effective control of Ebola virus infection is associated with balanced immune responses in survivors. Asymptomatic Ebola virus infection was demonstrated in humans during the 1996-97 disease outbreak in Gabon [16] . Asymptomatic infection was associated with an early strong inflammatory response that may be involved in the early inhibition of viral replication [16, 17] . Consistent with this discovery, we showed a decade later that a large fraction of the human population living in forested areas of Gabon has both humoral and cellular immunity to Ebola virus [18] . In the absence of identified risk factors, the high prevalence of 'immune' individuals suggests a common source of human exposure such as fruits contaminated by bat saliva.