What are the physiological effects of Ebola virus?Ebola virus disease is a rare but deadly disease that is transmitted through direct contact with blood or body fluids of infected people, bats or primates.

What are the physiological effects of Ebola virus?Ebola virus disease is a rare but deadly disease that is transmitted through direct contact with blood or body fluids of infected people, bats or primates.
What are the physiological effects of Ebola virus

Introduction
Ebola virus disease is a rare but deadly disease that is transmitted through direct contact with blood or body fluids of infected people, bats or primates. Upon exposure to the virus, symptoms will appear within 2 to about 21 days. Some of the symptoms are headache, diarrhea, hemorrhage, vomiting and severe fever. Ebola virus disease has an average fatality rate of 50 percent with some cases presenting with fatality rates of 90 percent (WHO, 2016). Most of the outbreaks have been reported in West Africa and both rural and urban areas being affected. In most cases, the recovery process would depend on the supportive clinical care and the immunity of the patient. Nonetheless, it is worth noting that the virus causes widespread destruction of the immune cells. Ebola virus infections have a myriad of physiologic events that eventually lead to systemic damage and eventually death. In this regard, it is prudent to highlight the events in order to shade light on the pathophysiologic changes that would be expected after infection with the Ebola virus. First, upon entry into the body, Ebola virus will target several immune cells in the body. The invasive nature will be the main process towards breaching the first line of defense. Secondly, the virus will then target specific organs that then become evident via a wide spread inflammation. Thirdly, the virus causes systemic hemorrhage (Sullivan, Yang, & Nabel, 2003).
The first physiologic effect upon entry of Ebola virus into the body is to break down the first line of defense. In this case, the virus will get into various cells of the immune system. The primary target are the dendritic cells thus making them defective. Defective dendritic cells will reduce the efficiency of T-lymphocytes to respond to further infections. With the defective T cells and the absence of antibodies will then make the virus to rapidly replicate and invade more cells (Sullivan et al., 2003). Furthermore, the virus will also proliferate and reproduce rapidly by inhibiting interferons. Ebola virus have been shown to use VP24 protein on their surface to bind to the immune cells and inhibit the role of interferon.
More physiologic effects are evident when the virus targets specific organs in the body. Other than targeting the immune cells, the virus will also target the liver, gastrointestinal tract and the adrenal glands (Sullivan et al., 2003). More changes in the physiology is indicated by wide spread inflammation that is as a result of destruction of cells or release of inflammatory cells. Direct invasion of organs such as the liver will result in inhibition of the processes that lead to the production of the coagulation proteins. Therefore, the patient is prone to hemorrhagic events (Centers for Disease Control and Prevention, 2015). More so, the virus will target cells within the gastrointestinal tract leading to diarrhea and the patient is subject to dehydration. Finally, the virus will invade the adrenal glands to cause a depletion of steroids. Depletion of steroids results in unregulated blood pressure and eventually a failure of the circulatory system.

Article 1
P, R., N, H., Md, V. K., J, L., J, W., Z, Y., … M, B. (2012). Clinical manifestations and case management of Ebola haemorrhagic fever caused by a newly identified virus strain, Bundibugyo, Uganda, 2007-2008., PloS One, 7, 7(12, 12), e52986–e52986.
The article highlights the clinical manifestations of Ebola virus disease that is caused by a newly identified virus stain. In this case, the new strain had been discovered at Bundibugyo in Uganda. Regarding the clinical manifestations, the new strain infection was characterized by non-bloody diarrhea in eighty one percent of the cases, severe headache in 81 percent and asthenia in approximately 77 percent of the victims. In most of the victims, the main physiologic change was hemorrhage that later resulted in fatalities. For instance, in seven of the observed case, there were six fatalities that occurred after the hemorrhagic process. The clinical fatality rate was 42 percent as a result of the infection by the new strain. In the outbreak, the average duration for the disease from appearance of symptoms was 9 days for the patients that died. Furthermore, the report indicated that there was increased risk of fatalities in cases where there were delayed hospitalization. The course of the disease was marked with fever, nausea and vomiting, abdominal pain, conjunctivitis and non-bloody diarrhea. The clinically notable hemorrhagic symptoms noted in the cases were melena and incidences of prolonged bleeding at the site of injection, hematuria, hemoptysis, hematoma, and postpartum vaginal bleeding. The study had setbacks such as limited data being collected.

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