Ebola Virus

Ebola virus (EBOV) is considered to be one of the most belligerent contagious agents and has an ability to cause highly fatal hemorrhagic fever syndrome that results in human and non-human primate’s death (NHPs) during the days of exposure. The first notification of the virus was mentioned in the Ebola River valley in Zaire for the time of an outburst in 1976. Moreover, the outbursts have appeared in Africa over the following 27 years, with death rates that differ from 50 to 90%.

In Central Africa, for the last three years outbursts have been recognized every year, the most recent of which proceeded in the Republic of the Congo with the amount of victims more than 125, according to the World Health Organization (“Ebola hemorrhagic fever. Information packet”, 2009). The precise derivation, positions, and natural habitats, which are also known as natural reservoirs of Ebola virus, continue to be unidentified.

Nevertheless, according to the available substantiation and the features of the same viruses, researchers claim that the virus is zoonotic (animal-borne), with 4 out of 5 subtypes that happen in animal hosts close to Africa. There is no doubt that similar hosts, mostly inhabited in the Republic of Philippines, are connected to the subtype named Ebola-Reston that was quarantined from contaminated cynomolgus monkeys, which were brought to Italy and the US from the Philippines. There is no likelihood that the Ebola exists on other continents such as North America (“Viral hemorrhagic fevers–Ebola and Marburg”, 2009).

It has been proven that the Ebola virus can be transferred from one human being to another by means of bodily contact. The common geographic territory considered being mostly influenced by divergent subtypes of the Ebola virus is Central Africa, especially the cities of Zaire, Sudan, and Gabon (Chepurnov, Bakulina, Dadaeva, Ustinova, & Chepurnova, 2009). Characteristically, Ebola virus infection runs its course from 14 to 21 days. Firstly, the infection can be identified with symptoms that are uncommon for the flu, including malaise, fever, and muscles pain.

With the progress of infection, patients experience acute bleeding and coagulation abnormalities such as a rash, gastrointestinal bleeding, and a big variety of hematological irregularities, for example neutrophilia and lymphopenia. Cytokines are discharged after reticuloendothelial cells confront virus, which can usually lead to exaggerated inflammatory responses that are not preventive. Detriment to the liver, together with heavy viremia, in most cases causes disseminated intravascular coagulopathy (Chepurnov, Bakulina, Dadaeva, Ustinova, & Chepurnova, 2009).

The following stage appears when the virus suddenly hits microvascular endothelial cells and damages vascular integrity. The final stages of Ebola virus infection traditionally involve diffuse bleeding, and hypotensive shock that lead to numerous Ebola virus fatalities. Ebola hemorrhagic fever, also known as Ebola HF, is an acute, mostly lethal disease that affects non-human and human primates, including gorillas, monkeys, and chimpanzees. The disease as well as the Ebola virus was firstly recognized in 1976.

It is considered to be difficult to diagnose Ebola HF on its early stages, namely in those people who have been contaminated only a few days. It can be explained, since early symptoms, including red eyes and a skin rash, are not specific for the virus and can be observed in other patients with diseases that appear much more often. Nevertheless, if a person has all the symptoms that have been mentioned, and infection with Ebola virus is suspected, it is recommended to quarantine the patient and report to the local and state health departments and the CDC (Dowell, Mukunu, Ksiazek, Khan, Rollin, & Peters, 1999).

The disease is a result of Ebola virus infection, which received its name after a river in the Democratic Republic of the Congo (earlier Zaire), Africa, where it was established for the first time. It is considered to be of RNA viruses that are named the Filoviridae and occurs in one out of two members of a family. On the whole, five determined subtypes of Ebola virus are distinguished. It is important to mention that four out of five subtypes lead to disease in human organisms only.

These four subtypes are Ebola-Ivory Coast, Ebola-Sudan, Ebola-Bundibugyo and Ebola-Zaire. The last subtype which is called Ebola-Reston results into disease in solely non-human primates such as monkeys, gorillas, chimpanzees. Soon after people get contaminated with the Ebola virus, it begins to accumulate within the body. Typically, Ebola virus symptoms become obvious in four to six days after receiving the infection. The period amidst getting infection and the beginning of symptoms is named the incubation period for the virus.

The incubation period for the Ebola virus can be very short such as 2 days as well as very long, namely 21 days. Furthermore, it has been proven that in pregnant women, typical symptoms of the Ebola virus can involve massive vaginal bleeding and abortion (miscarriage). In most cases death appears within the second week of the symptoms. It has been stated that sufferers of Ebola virus disease die from a heavy blood loss (Weingartl et al. , 2012). The infection is recognized by the primary signs of fatigue, fever, muscle aches, exhaustion, and dizziness.

With the progress of the disease, there appear massive bleeding under the skin, in inside organs, and from ears, eyes, and mouth. People who experience the acute development of the disease suffer from rapid symptoms of delirium, shock, seizures, coma, and nervous system malfunction (Peters, 1999). The Ebola virus can be diagnosed with the particular antigens discovered in blood samples, isolation of virus in cell cultures, or identification of IgM and IgG antibodies. ELISA (Enzyme-linked immunosorbent assay) tests are frequently utilized in order to identify viruses.

It should be mentioned that all tests are performed in the most rigorous laboratory conditions aiming to secure scientists and patients. There is considered to be no identified treatment for Ebola virus disease. Therefore, contaminated patients are treated by means of utilizing antiviral drugs, including ribavirin. Another method is a generally supportive therapy which restores endovenous fluids, keeps blood pressure in a good condition, and controls other bodily functions (Peters, 2005). Ebola itself has a usual length of 920 nm and a diameter of 80 nm.

The virus is considered being bio-hazardous at the level 4 and is only dealt with in the most sterile surroundings in totally secure suiting. Ebola is extended by means of direct contact with blood cells or other bodily release of contaminated people. Such closeness of infection makes outbursts around small communities and families very usual. Infection can also be a result of a contact with infected medical equipment, including glassware, needles, not sterile equipment, or negligent laboratory procedures (“Ebola hemorrhagic fever in Zaire”, 1978).

One of the common features of the infection with the Ebola virus is the damage to the immunity. The vast majority of diseased people are not capable of developing adequate immune responses. In most cases it is connected to the virus’s infection of the fibroblastic reticular system that plays a crucial role in immune system improvement. A group of scientists claim that malfunction of cytokine production is a result of the infection of both fibroblastic reticular system and mononuclear phagocytes, additionally to the malfunction of antigen trafficking.

Furthermore, within that spread of virions amidst tissues is, to a limited extent, due to the infection from macrophages and circulating monocytes (“Ebola hemorrhagic fever in Sudan”, 1978). One of the initial deficiencies of the immune system concerning the Ebola virus is the incapability to activate T-cells early in the course of the infection, resulting in an insufficient humoral response that involves both antibody and cytokine responses. Another effect of the deficiency of sufficiently activated T-cells is apoptosis of blood leukocytes.

These features of Ebola infection are generally connected to death in patients. In both lethally contaminated patients and experimentally contaminated monkeys, the virus appeared to result in massive destruction of spleen, lymph nodes, and bone marrow. Patients who overcame infection by Ebola virions were capable of developing stronger antibody responses at the early stages of the infection than patients who suddenly resorted to the disease. Few years ago, a protein known as cyanovirin-N was found in blue-green algae and it became connected to Ebola virus.

The drug has been discovered in order to partly subdue the ability of Ebola to unite and contaminate cells, resulting in the host’s survival time expansion. What is more, cyanovirin has been discovered in order to unite the outside cells that gave chances of inhibiting their ability to cross the cellular membranes. Cyanovirin appears to be a very promising drug that gives the ability to attach to sugar molecules discovered on the surface of Ebola virus. Those experiments concerning cyanovirin have been conducted by means of animal models, in which test animals were contaminated with Ebola and given injections of cyanovirin once a day.

The experiment lead to a hold-up in the beginning of the disease and longer survival in those animals injected with the protein than in those that were not injected (Murphy, 1978). The preventive methods of Ebola HF in Africa face numerous challenges. It happens, since the originality and location of the natural reservoir of Ebola virus are unexplored. Consequently, there are only few minor established initial preventive measures.

References Centers for Disease Control and Prevention. (2009). Ebola hemorrhagic fever.Information packet. Retrieved from http://www. cdc. gov/ncidod/dvrd/spb/mnpages/dispages/Fact_Sheets/Ebola_Fact_Booklet. pdf The Center for Food Security and Public Health. (2009). Viral hemorrhagic fevers–Ebola and Marburg. Retrieved from http://www. cfsph. iastate. edu/Factsheets/pdfs/viral_hemorrhagic_fever_filovirus. pdf Chepurnov, A. , Bakulina, L. , Dadaeva, A. , Ustinova, E. , & Chepurnova, T. (2009).

Inactivation of Ebola virus with a surfactant nanoemulsion. Transfusion, 49(Suppl. ), 72-74. Retrieved from http://www.aabb. org/resources/bct/eid/Documents/72s. pdf Dowell, S. F. , Mukunu, R. , Ksiazek, T. G. , Khan, A. S. , Rollin, P. E. , Peters, C. J. and the Commission de Lutte contreles Epidemies a Kikwit. (1999). Transmission of Ebola hemorrhagic fever: A study of risk factors in family members, Kikwit, Zaire. The Journal of Infectious Diseases, 179 (Suppl. 1), 87-91. Retrieved from http://jid. oxfordjournals. org/content/179/Supplement_1/S87. full International Study Team. (1978). Ebola hemorrhagic fever in Sudan, 1976.

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