Figure 1.

A schematic representation of Ebola virus (EBOV) pathogenesis. The virus is capable of productively infecting monocytes, macrophages, dendritic cells (DC) (except epidermal, mucosal and CD141⁺ DC) and hepatocytes. The virus does not enter lymphocytes but can show interaction with CD4⁺ T-cells. Despite non-entry into lymphocytes, bystander lymphocyte apoptosis is observed during the course of infection which could lead to T-cell exhaustion. Infection of hepatocytes could result in downregulation of blood coagulation enzymes which could lead to hemorrhage. Severe infection leads to hyperproduction of proinflammatory cytokines. These cytokines activate coagulation factors such as thrombomodulin, ferritin etc. The released coagulation factors in turn upregulate proinflammatory cytokines, as depicted. Hence, a deadly chain reaction ensues upon filoviral infection which might culminate into shock, vascular damage (disseminated intravascular coagulation which might lead to hemorrhage especially rashes, gastrointestinal and conjunctival hemorrhage in the later stages) and homeostatic imbalance.