Cellular Pathogenesis

3. What organs are effected and how?

The pathological changes have been noticed in patients dying with all filovirus infections, with extensive necrosis in parenchymal cells of many organs, including liver, spleen, kidneys, gonads and so forth (Zakin et al., 1999). In terms of organ infectivity titer, testis, lymph nodes, spleen, adrenal gland and liver have higher PFU/ml than other organs (Geisbert, 2003). This maybe linked to the abundance of macrophages in these organs tissue, where this tropism likely plays an equally important role in the disease pathogenesis.

Liver
The liver is one of the important organ affected by EBOV arising from abundant macrophages. Various degrees of hepatocellular degeneration have been reported in filovirus infections of humans and nonhuman primates. (Geisbert et al., 2003; Jaax et al., 1996; Ryabchikova et al., 1999). Therefore, the impairment of the liver may explain the overall pathogenesis as hemorrhagic tendencies in certain cases related to decreased synthesis of coagulation factors and other plasma proteins as a result of severe hepatocellular necrosis.

Impairment of

Remarkable platelets reduction and D-dimers increase were observed in animal model (Geisbert et al., 2003), probably related to the liver damage. However, massive loss of blood is infrequent and, when present, is primarily limited to gastrointestinal tract. In fact, the amount of blood that is lost is unusual to cause death. (Knipe et al., 2013) The mechanism responsible for triggering the coagulation disorder is not completely understood. Research studies suggest that extensive viral replication induce overexpression of IL-6, resulting in the excessive activation of coagulation cascade (Geisbert et al., 2003). Thus, the liver may not be able to synthesize sufficient amount of coagulation factors in time and leading to further organs damage and hemorrhagic shock.Adrenal