- "In infected dendritic cells (DCs), Ebola virus replicates efficiently and inhibits DC maturation without inducing cytokine expression, leading to impaired T-cell proliferation.
During infection, monocytes/macrophages in the lymphoid tissues are early and sustained targets of this deadly virus. Since these cells usually elicit the response cascade in the acute phage of inflammation, their early infection helps Ebola evade the immune system while subsequently spreading throughout the host.
In addition, infected macrophages release increased amounts of nitric oxide (NO), a gaseous hormone that normally functions in cell communication. However, in high concentrations, NO depresses the mitochondrial membrane potential, causing apoptosis in nearby natural killer cells  (Fig 12).
So far, most of the processes by which Ebola escapes or hampers immune response involve viral structure proteins.
However, other studies have implicated a role of sGP in immune system evasion.
During viral infection, large amounts of proinflammatory cytokines like tumor necrosis factor alpha (TNF-α) are secreted from infected macrophages and cause disruption of the endothelial barrier (Fig 12). Surprisingly, when sGP was administered simultaneously with TNF-α, it caused a recovery of barrier function .
(Comment. sGP is a real blackguard, a snake in the grass)
This suggests an anti-inflammatory role of sGP that helps to explain somewhat mysterious observations during infection. When a patient is suffering from Ebola, tissue destruction can be seen in multiple organs. However, these areas are not infiltrated by leukocytes, which instead appear to congregate within the adjacent vascular system. It appears that the recruitment of neutrophils via an activated endothelium has occurred, but the transmigration process is blocked by the anti-inflammatory effect of sGP .
In addition, sGP shares many neutralizing epitopes with GP, suggesting that this secreted protein may serve as a decoy that absorbs antibodies  (Fig 12).