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Ebola and Marburg Viruses Ebola and Marburg Viruses: Description Ebola is a member of negative-stranded RNA virus family Filoviridae. Ebola and Marburg viruses (filo viruses) are very similar in density, morphology, and odium dodecyl sulfate - polyacrylamide gel electrophoresis (SDS-PAGE) profile. As far as these particles are pleomorphism, it means that they can exist in many shapes. The Marburg virus is the causative agent of Marburg hemorrhagic fever. It relates to Ebola, and was first discovered in Eastern Congo and Uganda. The zoonosis is of unknown origin.
Ebola is the common term that is used to describe a group of viruses that belong to genus Ebola virus, family Filoviridae. The Ebola viruses are very similar to the Marburg virus, and share very similar disease symptoms. The basic structure of the Ebola and the Marburg viruses is filamentous and long. It is essentially bacilli form, but both viruses relatively often taken on a "U" shape. The particles are up to 14, 000 nm in length and average 80 nm in diameter. The Ebola and the Marburg viruses consist of a nucleocapsid, which is surrounded by a cross-striated helical capsid.
The nucleocapsid has an axial channel, and the virion is surrounded by a lipoprotein unit derived from the host cell (Ebola and the Marburg viruses). The genome comprises of a non-infectious, non-polyadenylated single negative strand of RNA. The arrangement of genes is linear, with some overlaps. The order is as follows: 3 '-untranslated region, nucleoprotein, viral structural protein, VP 35, VP 40 glycoprotein, VP 30, VP 24, polymerase (L), 5 '-untranslated region (Ebola and the Marburg viruses). It is still unknown the mechanism how the virus enters the cell.
However, after the virus enters the cells, it transcribes the RNA in cell and replicates in the cytoplasm of the infected cell. The replication of the virus is mediated by the synthesis of an antisense positive RNA strand; - this mechanism will be used further as a template for additional viral genomes. The virus progresses the cytoplasm of the infected cell and develops prominent inclusion bodies containing highly structured viral nucelocapsid. Then the virus assembles, buds off the host cell, and attains the cells lipoprotein coat from the outer membrane of the infected cell. The Marburg virus was named after Marburg, the town in Germany, where the first cases of disease were described.
Ebola virus was named for a small river not far from Marine, Sudan. Since 1967 there have been more than 1, 000 cases of Marburg and Ebola, with over 50 % of the patients dying within few days on the onset of the acute symptoms of the disease. Similar to Marburg virus, Ebola virus is classified as a biosafety level 4 agent due to its extreme pathogenicity as well as the lack of antiviral drug or vaccine. Ebola Zaire is the most highly virulent subtype of Ebola virus. The infection leads to the patient's death. This virus first appeared in 1972; however, it was not properly identified until the later cases of disease that took place in 1976.
Ebola Sudan is also extremely pathogenic subtype of Ebola virus. It was first discovered in 1976 along with the 1976 epidemic Ebola Zaire. Ebola Reston is another pathogenic subtype of Ebola virus. It was originated in Asia and was later brought to Italy and the United States through the infected macaques that were imported from Philippines. The mortality among the infected monkeys was about 80 percent. Ebola Reston has not yet resulted in death in humans, although it was observed in at least four people.
Ebola-Tai is quite a new strain that occurred in 1994 and was further examines as the unique subtype of Ebola virus in 1995 at the Institute Pasteur, Paris. This subtype of virus was the first recognized emergence of Ebola in West Africa. Ebola and Marburg Viruses: Location Endemic areas for Marburg Virus are Central and East Africa. One of the most endemic areas is the Mt. Elgon region, on the border of Uganda and Kenya, and Zimbabwe. What concerns Ebola virus, the endemic areas are Africa and Asia.
Similar to Marburg Virus, the most fertile' area for the virus is the Mt. Elgon region. There is an assumption, that Ebola virus has quite wide geographic distribution, where monkeys play an essential role, in the capacity of host species to the unknown arthropod vector. According to the studies, about 10 percent of all African and Asian monkeys tested carry Ebola antibodies.
Ebola and Marburg Viruses: Vector The natural reservoir for Ebola virus is still unknown. However, there is an assumption that the natural reservoir is a part of rural African areas, and, as it was already mentioned, 10 % of all African and Asian monkeys have antibodies to filo viruses. The secondary spread of the disease occurs through contact with blood, secretions, or excretions of the infected persons. The infection rate that occurs due to contact with the viremic persons is not high, as it makes up about 10 percent, thus being conductive to the assumption that the contact with infected persons is not an efficient form of transmission of the disease caused by this virus. It is also noted that nosocomial transmission is more dangerous, as in all epidemics, this type of transmission that occurred mainly through contaminated needles or syringes, was responsible for the highest death rates. At the same time, there were some cases in Sudan and Zaire where the patients had no contact with body fluids or the blood of the infected patients.
There is an assumption that these patients were infected through aerosol transmission. At the same time, although the Sudan and Zaire strains are not passed from human to human via aerosol transmission, the Reston strain can be transmitted through small-particle aerosol from monkeys to humans. It was also found that the Ebola virus can persist in dried material, multimode medicine vials, and injection equipment. It may also be found in the patients semen for three or four months after the general symptoms of the disease disappeared. What concerns Marburg virus, the natural reservoir for this virus is also unknown. Similar to Ebola virus, there is an assumption that the natural reservoir for Marburg virus is a part of rural African areas.
Similar to Ebola virus, the secondary spread of the disease caused by Marburg virus usually occurs through the contact with the infected persons, and contact with their secretions, blood, or excretions. The virus can also be found in the semen of the infected patient for three or four months after the general symptoms of the disease disappeared. However, the sexual transmission of Marburg virus was reported in one case only in Germany (Marburg virus). Ebola and Marburg Viruses: Mechanism For both viruses, the exact mechanism is still unknown. Yet, for Marburg virus, the surface spikes of the virus are made solely of large glycoprotein, and there is an assumption that, similar to the mechanisms for other negative-strand RNA viruses, the surface spikes of the virus tend to bind to the receptors on the host cell and then mediate entry into susceptible cells. The Marburg virus has 22 potential N-linked glycosylation sites on the surface (Marburg virus).
The replication of the virus occurs in the cytoplasm. The envelopment occurs as a result of the budding preformed nucleocapsid's. It is also found that Marburg virus affects liver, lymphoid organs, and kidneys. Similar to the Marburg virus, the exact mechanism of Ebola virus is unknown. It is known that Ebola virus involves blood vessels, the heart, stomach, liver, intestine, lymphoid organs, and kidneys, and causes hemorrhaging. In many cases the virus leads to organ failure.
The person usually dies without the evidence of the immune response (Ebola virus). There are several assumptions concerning the possible mechanisms of the virus. On the surface Marburg virus has 22 potential N-linked glycosylation sites, while Ebola virus has 17 potential N-linked glycosylation sites on its surface. Both viruses have 7 genes that code for protein. It was also found that one gene codes for 2 variations of the same glycoprotein (GP): a smaller (sGP) form and a transmembrane glycoprotein (GP). The surface spikes of the Marburg virus comprise of that large glycoprotein, and the Ebola surface spikes are similar to that of Marburg virus (Ebola virus).
Both, large and small forms of glycoprotein are secreted from the infected cells. Both proteins are encoded by the same gene, however, the proteins have different cellular targets (Ebola virus). The smaller protein that is at least 300 anime acids smaller than the larger one, is secreted during the early phases of the disease. This protein then binds to the white blood cells (neutrophils) that trigger inflammation. There is an assumption that the smaller protein locks up and halts the inflammatory response which should fight off the virus (Ebola virus). In its turn, the larger membrane GP is bound to the Ebola virus.
This membrane GP is proved to form the surface of the new viruses that are created in the cells infected by Ebola virus. The studies in animals have shown that this membrane GP invades numerous types of cells. Yet, this GP was found to bind predominantly to the receptors on endothelial cells that line the inner surfaces of the blood vessels, heart, and other internal organs. Then, this binding makes possible for the GP surface spikes to mediate their entry into susceptible cells. After entering into the cells, the virus then replicates in the cytoplasm. However, it should be taken into account that all these mechanisms are only hypotheses, as the mechanism is still unknown.
Ebola and Marburg Viruses: Diseases As it was already mentioned, the diseases caused by these viruses are Marburg hemorrhagic fever and Ebola hemorrhagic fever. The incubation period for the Marburg virus lasts about 5 - 7 days, however, it may vary from 3 - 10 days. What concerns Ebola virus, the average incubation period lasts for 5 - 7 days for nosocomial transmission, and for close-contact transmission it may last about 6 - 12 days. The symptoms Ebola virus infection is quite similar to that of Marburg, as it includes sudden onset of fever, malaise, involving extreme prostration and even weight loss. The subsequent symptoms include chest pain, sore throat, skin rash, abdominal pain, and diarrhea. The blood of infected patient fails to clot.
The excessive effusions from the infected patients internal organs may occur, followed by renal dysfunction and pulmonary interstitial edema. Approximately 15 percent of patients infected with Ebola Zaire experience hic cubs, and 38 percent develop bleeding. After 7 - 10 days the patients who will survive from the Ebola virus begin to recover. The period of recovery may last about five weeks or more, and may be followed by the weight loss, prostration, and amnesia.
Those patients infected with Ebola virus with the highest risk of dying, have extensive of diffuse hemorrhage into the mucous membranes, skin, as well as internal organs. Swelling of the lymph nodes, spleen, brain and kidneys also takes place. There is also an evidence of interstitial pneumonia, inflammation in the patients eyes, and pancreatitis. By the end of the first week of the acute symptoms of the disease, the patients begin to vomit a black "sludge" of blood and disintegrated internal organs (Ebola virus). The capillary leakage then leads to a vascular collapse, and the patient experiences coma and convulsions, and then death occurs. As it is reported, the mortality rate is about 90 percent.
What concerns Marburg virus, the infected patient first experiences the symptoms similar to the fever caused by Ebola virus. The fever usually lasts about seven days. On the fifth day, maculopapular petechia l rash appears and the patient experiences hemorrhaging. The subsequent symptoms include myalgia, headaches, inflammation of the eyelid and eye membrane, liver, and intestine. Within 7 - 10 days the patients, who will survive, begin to recover. The recovery usually lasts about five or more weeks, and is followed by weight loss, prostration, and amnesia (similar to the fever caused by Ebola virus).
Those patients who will die, have diffuse or extensive hemorrhage into their internal organs, mucous membranes, skin, intestines, and stomach. Then, the swelling of lymph nodes, spleen, and brain occurs. The patients then have coma and convulsions, followed by death that occurs usually in 6 - 9 days after the clinical onset of typical symptoms of the disease. Ebola and Marburg Viruses: Treatment, Prevention, and Research It should be taken into account that there is no specific therapy for treating Ebola and Marburg hemorrhagic fevers. What concerns Marburg hemorrhagic fever treatment, the virus is sensitive to detergents, lipid solvents, phenolic disinfectants, and commercial hypochlorite disinfectants. It can also be destroyed by gamma radiation and ultraviolet radiation.
What concerns Ebola hemorrhagic fever treatment, the patients are offered supportive therapy. The fluids pumped into the bloodstream usually leads to the patients death by pulmonary edema, because the leaking veins in the lungs flood the airways with fluid (Ebola virus). What concerns prevention, there are vaccines for both Ebola and Marburg viruses based on recombinant Adenovirus that carries the Ebola spike protein on its surface or a recombinant Vesicular stomatitis virus. However, early human vaccine efforts (i. e. at NIAID in 2003) were met with no success.
In such a way, preventive strategies are not successful. The research groups consistently work on vaccines and drugs able to fight the viruses. A group of scientists from the United States Army Medical Research Institute of Infectious Diseases (USAMRIID) (1998) has published the first article about the development of the first experimental Marburg virus vaccine. In 2002, another research company that worked for the United States Army's biodefense program reported successful experiment in animals. In 2003 the U. S.
government has awarded that company a contract for a multivalent Ebola, Marburg filo virus vaccine program. Later, in 2005 the researchers from Canada's National Microbiology Laboratory reported that they developed a vaccine that was highly efficient in case it was administered shortly after a patient is infected. Yet, the scientists still continue their efforts to develop a vaccine that will be 100 % effective for treatment even if the patient experiences acute symptoms. Works Cited Harper, Tara K. "TKH Virology Notes: Ebola. " 2005. 6 December 2007 < web >... "TKH Virology Notes: Marburg Hemorrhagic Fever. " 2004. 6 December 2007 < web >. Old stone, Michael B.
A. Viruses, Plagues and History. Oxford: Oxford University Press, 2000.
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Research essay sample on Ebola And Marburg Viruses
