Scientists struggle to find successful interventions to the Ebola virus.

One of the focuses of research is

the ability of the Ebola virus to interfere with the functionality of the human immune system. The
human body produces proteins called cytokines that activate cells to fight pathogens that enter the
body (Whicher & Evans, 1990). In some instances the body generates too many cytokines which is
counterintuitive. The basis/pathogen of this overproduction of cytokines determines the intensity of this
phenomenon. In milder cases this is seen in diseases such as influenza, rheumatoid arthritis or psoriasis
(Kunz & Ibrahim, 2009). In more extreme cases such as the Ebola virus, a cytokine storm ensues which
leads to fever, fluid retention, weakened lining of arteries/veins, tissue death, sepsis, etc. (Clark, 2007).
In essence, as with other autoimmune diseases, the Ebola virus has the human body attack itself.
Ebola leads to sepsis in rapid fashion. Sepsis is severe infection and inflammation throughout the body.
With sepsis the body cannot deliver blood (low blood pressure) and organs fail. Overall, the medical field
does not have a handle on managing sepsis in general (Angus & Van der Poll, 2013). This is a key factor
in tackling the Ebola virus. However, sepsis treatment is to be started within 6 hours of onset (Angus &
Van der Poll, 2013), yet the Ebola virus can hide symptoms until the disease is already widespread in the
body. Sepsis also requires intensive treatment with contemporary intervention (Angus & Van der Poll,
2013) that is not typically available in many areas of Africa where most Ebola victims are located. Unless
sepsis treatment is readily available in remote locations, many people will continue to die. Ideally the
Ebola virus source must be eliminated, an immunization discovered or development of an effective
treatment to be used prior to sepsis development.

Sources:
Angus, C. & Van der Poll, T (2013). Severe Sepsis and Septic Shock. The New England Journal of
Medicine. vol. 369 p. 840-851. Retrieved from
http://www.nejm.org/doi/full/10.1056/NEJMra1208623#t=article.
Clark, I. (2007). The advent of the cytokine storm. Immunology and Cell Biology vol 85, p 271-273.
Retrieved from http://www.nature.com/icb/journal/v85/n4/full/7100062a.html
Kunz, M. & Ibrahim, S. (July 2009). Cytokines and Cytokine Profiles in Human Autoimmune Diseases and
Animal Models of Autoimmunity. Mediators of Inflammation vol, 2009, Article ID 979258.
Retrieved from http://www.hindawi.com/journals/mi/2009/979258/
Tracey, K. (February, 2007). Physiology and immunology of the cholinergice anti-inflammatory
pathyway. The Journal of Clinical Investigation. vol.117. no. 2. Retrieved from
http://www.jci.org/articles/view/30555/version/1/pdf/render
Whicher, J.T. and Evans, S.W. (1990) Cytokines in Disease. Clin. Chem. 36/37, 1269-1281. Retrieved from
http://www.clinchem.org/content/36/7/1269.full.pdf