Ebola Virus Disease: Understanding the Current Outbreak
Ebola Virus Disease: Understanding the Current Outbreak
The Ebola virus enters the human chain through close contact with the bodily fluids of primates and other animals, including chimpanzees, gorillas, fruit bats, monkeys, forest antelope, and porcupines found ill or dead in the rain forest. It can then be transmitted human to human through the mucous membranes, via tears in the skin, by direct contact with the infected person's bodily fluids, or parenterally. The virus can also be spread by direct contact with the body of a deceased individual who was infected with the Ebola virus. Males can transmit the virus through their semen for up to 7 weeks following recovery. A natural host for the Ebola virus has not yet been identified; therefore, it is difficult to control the spread of the virus.
The incubation period depends upon the route of infection, where parenterally infected individuals will show symptoms quicker than those infected by contact. The virus travels from the site of infection to the regional lymph nodes, liver, spleen, and adrenal glands. In the human body, the virus can infect monocytes, macrophages, dendritic cells, endothelial cells, fibroblasts, hepatocytes, adrenal cortical cells, and epithelial cells. Although the lymphocytes are not infected, they undergo apoptosis and therefore their numbers are reduced.
It has been demonstrated that both the host and the viral proteins contribute to the pathogenesis of the Ebola virus. The virus seems to trigger the release of inflammatory cytokines, lpha, interleukin-2 (IL-2), IL-10, andαinterferon (IFN)-γ, IFN- tumor necrosis factor (TNF)-α, which leads to subsequent vascular leak and clotting, ultimately resulting in multiorgan failure and shock.
Hepatocellular necrosis, combined with massive viremia, leads to dysregulation of clotting factors and disseminated intravascular coagulopathy. In some cases, the adrenal cortex is affected, leading to hypotension and impaired steroid synthesis.
Pathogenesis
The Ebola virus enters the human chain through close contact with the bodily fluids of primates and other animals, including chimpanzees, gorillas, fruit bats, monkeys, forest antelope, and porcupines found ill or dead in the rain forest. It can then be transmitted human to human through the mucous membranes, via tears in the skin, by direct contact with the infected person's bodily fluids, or parenterally. The virus can also be spread by direct contact with the body of a deceased individual who was infected with the Ebola virus. Males can transmit the virus through their semen for up to 7 weeks following recovery. A natural host for the Ebola virus has not yet been identified; therefore, it is difficult to control the spread of the virus.
The incubation period depends upon the route of infection, where parenterally infected individuals will show symptoms quicker than those infected by contact. The virus travels from the site of infection to the regional lymph nodes, liver, spleen, and adrenal glands. In the human body, the virus can infect monocytes, macrophages, dendritic cells, endothelial cells, fibroblasts, hepatocytes, adrenal cortical cells, and epithelial cells. Although the lymphocytes are not infected, they undergo apoptosis and therefore their numbers are reduced.
It has been demonstrated that both the host and the viral proteins contribute to the pathogenesis of the Ebola virus. The virus seems to trigger the release of inflammatory cytokines, lpha, interleukin-2 (IL-2), IL-10, andαinterferon (IFN)-γ, IFN- tumor necrosis factor (TNF)-α, which leads to subsequent vascular leak and clotting, ultimately resulting in multiorgan failure and shock.
Hepatocellular necrosis, combined with massive viremia, leads to dysregulation of clotting factors and disseminated intravascular coagulopathy. In some cases, the adrenal cortex is affected, leading to hypotension and impaired steroid synthesis.
Source...