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. Author manuscript; available in PMC: 2012 Jul 26.
Published in final edited form as: Lancet. 2011 Mar 5;377(9768):849–862. doi: 10.1016/S0140-6736(10)60667-8

Figure 2. Model of Ebola virus pathogenesis.

Figure 2

Virus spreads from the initial infection site (small lesions) to regional lymph nodes, liver, and spleen. Although Ebola virus does not infect lymphocytes, their rapid loss by apoptosis is a prominent feature of disease. The direct interaction of lymphocytes with viral proteins cannot be discounted as having a role in their destruction, but the substantial loss of lymphocytes probably results from a combination of factors including infection-mediated impairment of dendritic cells and release of soluble factors from monocytes and macrophages. Soluble factors released from target cells also contribute to the impairment of the vascular system leading to vascular leakage as demonstrated here in cultures of endothelial cells (white arrowheads). The systemic virus spread and replication, the general dysregulation of the host immune response, the coagulation abnormalities, the impairment of the vascular system, and hypotension all together finally result in shock and multiorgan failure. IL=interleukin. MCP-1=monocyte chemoattractant protein-1. MIPs=macrophage inflammatory proteins. NO=nitric oxide. TNFα=tumour necrosis factor α.