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Ebola Virus Essay, Research Paper

Please Read This Warning Before You Use This Essay for Anything (It Might Save Your Life) Ebola VirusThe Ebola Virus is the common name for several strains of virus, threeof which are known to cause hemorrhagic fever in humans, which ischaracterized by massive bleeding and destruction of internal tissues.Named for the Ebola River in Zaire, Africa, where the virus was firstidentified, the Ebola virus belongs to the family Filoviridae. Threestrains of Ebola virus that are often fatal to humans have beenidentified. Named for the areas in which the first recognized outbreakstook place, these strains are referred to as Ebola/Zaire (EBOZ),Ebola/Sudan (EBOS), and Ebola/Tai Forest (EBOT). A fourth Ebola strain,called Ebola/Reston(EBOR), has not been found to cause disease inhumans. As outbreaks of Ebola hemorrhagic fever continue to occur,other strains may be identified. The viruses are long rods, 800 to1000 nanometers (nm) long (1 nm equals one-billionth of a meter, or 4 x10-8 in), but particles as long as 14,000 nm have been seen. Each virusconsists of a coiled strand of ribonucleic acid (RNA) contained in anenvelope derived from the host cell membrane that is covered with 7 nmspikes placed 10 nm apart visible on the surface of the virion (Figure1). When magnified several thousand times by an electron microscope,these viruses have the appearance of long filaments or threads but theparticles are pleomorphic, meaning they can exist in many shapes. Theirbasic structure is long and filamentious, essentially bacilliform, butthe viruses often takes on a “U” shape (Figure 2). They contain aunique single-stranded molecule of noninfectious (negative sense ) RNA.The virus is composed of 7 polypeptides, a nucleoprotein, aglycoprotein, a polymerase and 4 other undesignated proteins. Proteinsare produced from polyadenylated monocistronic mRNA a speciestranscribed from vi genomes. As the infection progresses the cytoplasm of the infected celldevelops “prominent inclusion bodies” which contains the viralnucelocapsid, which will become highly structured. The virus thenassembles, and buds off the host cell, attaining its lipoprotein coatfrom the infected cell’s outer membrane. The replication in anddestruction of the host cell is rapid and produces a large number ofviruses budding from the cell membrane. Symptoms Cases of Ebola haveoccurred in isolated instances and in outbreaks in sub-Saharan Africa.A significant problem in diagnosing the disease is that the virusesoften strike in remote areas of developing countries, where access tolaboratories for specimen analysis is limited. Of all the Ebolastrains, Ebola/Zaire is the most dramatic and deadly. The Ebola viruscauses hemorrhagic fever, which is characterized by such symptoms assevere headache, weakness, and muscle aches, followed by vomiting,abdominal pain, diarrhea, inflammation of the throat (pharyngitis),inflammation of the mucous membranes in the eye (conjunctivitis), andbleeding from body openings. The virus spreads through the blood and isreplicated in many organs. The histopathologic change is focal necrosisin these organs, including the liver, lymphatic organs, kidneys,ovaries and testes. The central lesions appear to be those affectingthe vascular endothelium and the platelets. The resultingmanifestations are bleeding, especially in the muc usually seven to tendays. The mortality rates in the known outbreaks have been 60 percent with Ebola/Sudan virus and 77 to 88 percent with Ebola/Zairevirus. Although it is believed that death results directly from thedamage to internal tissues, it is not known why some patients manage tosurvive the disease. There are no proven therapeutic drugs to treatEbola hemorrhagic fever, and treatment currently consists of preventingshock and providing supportive care. Medical care is complicated by theneed to protect medical and nursing personnel. Convalescence is slow,often taking five weeks or more, and is marked by weight loss andamnesia in the early stages of recovery. Currently, there is littlehope of developing a vaccine against the Ebola virus. Near the end ofone outbreak in Zaire during 1995, blood from convalescent patients wastransfused into severely ill victims in an attempt to transferantibodies and T-lymphocytes (one type of white blood cell) that mightneutralize the Ebola virus and destroy infected cells. This proceduremet with some success, but carefully controlled trials must beconducted to confirm the safety and effectiveness of this method.Evolution Besides morphological and biochemical similarities, allnonsegmented negative-strand RNA viruses share several features intheir mechanisms of transcription and replication: similar genomeorganization, complementarity of the genome extremities, homologoussequences in the 3′ untranslated region, conserved transcriptionalsignals, interruption of genes by intergenic sequences, possession of avirion-associated polymerase, helical nucleocapsid as the functionaltemplate for synthesis of replicative and messenger RNA, replication bysynthesis of a full-length antigenome, transcription of messenger RNAsby sequential interrupted synthesis from a single promotor,transcription and replication in the cytoplasm, and maturation byenvelopment of independently assembled nucleocapsids at membrane sitescontaining inserted viral proteins. These data suggest that allnonsegmented negative-strand RNA viruses are derived from a commonprogenitor and support the classification of the families Filoviridae,Paramyxoviridae and Rhabdoviridae in the order Mononegavirales. Inaddition, comparative amino acid sequence analyses of nucleoproteinsand polymerase proteins suggest that filoviruses are more closelyrelated to paramyxoviruses than to rhabdoviruses. History of EbolaOutbreaks Ebola virus was identified for the first time in 1976, whentwo epidemics of hemorrhagic fever occurred, one in Zaire, the other600 km distant in Sudan. The combined outbreaks accounted for morethan 550 cases and 430 deaths. A third strain of the Ebola virus wasidentified in 1989 in a quarantine facility in Reston, Virginia, wherehundreds of imported Philippine monkeys died. The Ebola/Reston virusseems not to cause disease in humans-although four laboratorytechnicians were infected with the virus, none of them became ill.Another large epidemic of Ebola hemorrhagic fever occurred in Zaire,this time in and around the city of Kikwit during the summer of 1995,infecting 315 people and killing 242. The strains of Ebola virusisolated in Zaire in 1976 and 1995, 19 years and 500 km apart, arevirtually identical. A single nonfatal case of Ebola hemorrhagic feveroccurred in late 1994 in Cte d’Ivoire. A Swiss zoologist who performedan autopsy on a chimpanzee was infected by the virus, which wassubsequently identified as the fourth strain, Ebola/Tai Forest, namedfor the Tai Forest in the Cte d’Ivoire. Since the first episode therehave been additional cases and fatalities caused by this virus, in Cted’Ivoire, Liberia, and Gabon. Diagnosing the Virus Each outbreak hasbeen traced to an index case, an infected person who came into contactwith a reservoir host, an animal or arthropod involved in the lifecycle of the virus. Of all the disease-causing human viruses, the Ebolaand its relative Marburg, which also causes hemorrhagic fever, are theonly ones remaining for which the original host and the naturaltransmission cycle remain unknown. It is not known whether monkeysserve as hosts or if other mammals, birds, reptiles, or even mosquitoesor ticks are involved. >From the index case, infection between humansis principally due to direct, close contact, such as that between apatient and nurses and doctors. Unhygienic hospital conditions alsospread the virus. The disease is diagnosed using a laboratorytechnique called ELISA (enzyme-linked immunosorbant assay) thatsearches for specific antigens (viral proteins) or antibodies made bythe infected patient. The test is performed on a monolayer of infectedand uninfected cells fixed on a microscopic slide. IgG- or IgM-specificimmunoglobulin assays are performed. These tests may then be confirmedby using western blot or radioimmunoprecipitation. Virus isolation isalso a highly useful diagnostic method, and is performed on suitablypreserved serum, blood or tissue specimens stored at -70oC or freshlycollected. A technique used to duplicate genetic material for study,called the polymerase chain reaction, is used to detect Ebola viralmaterial in patient blood or tissues. When infection by the virus issuspected, local health officials institute strict barrier nursingprocedures (such as the use of gowns, gloves, and masks) and usually

call on experts from the World Health Organization (WHO), the Centersfor Diseas The Ebola virus has been classified by the CDC as BiosafetyLevel 4, which requires the greatest safety precautions. To ensuremaximum safety, virologists must work in special protective clothing,and their laboratories contain equipment that sterilizes air, andliquid and solid wastes. Detailed studies comparing RNA sequencesbetween the different viral strains are only now being performed. It ishoped that such genetic information will provide clues about thenatural history and hosts of the viruses. Natural Reservoir Thenatural reservoir of the Ebola virus is not entirely known. Serologicalstudies suggest that Ebola or related viruses are endemic in Zaire,Sudan, the Central African Republic, Gabon, Nigeria, Ivory Coast,Liberia, Cameroon and Kenya. The geographic range of Ebola strains mayextend to other African countries, for which adequate survey islacking. Extensive ecological studies are currently underway in Cted’Ivoire, Gabon and Zaire to pinpoint the reservoir. Ebola-relatedfiloviruses were isolated from cynomolgus monkeys (Macaccafascicularis) imported into the United States of America from thePhilippines in 1989. A number of the monkeys died and at least fourpersons were infected, although none of them suffered clinicalillness. Annalysis of Outbreaks Serologic evidence has suggested thepresence of Ebola virus in Gabon since 1982. Since late 1994, threeapparently independent outbreaks of Ebola virus hemorrhagic fever haveoccurred among humans in northeastern Gabon, in the forested areas ofequatorial Ogoou-Ivindo province. The first, which started in December1994 in gold-panner encampments of far northeastern Gabon, in theMinkouka area (Figure 3) near the Nouna River, had severallaboratory-confirmed cases. The second, which began in early February1996 in Mayibout village (Figure 3) on the Ivindo River, resulted in 37Ebola hemorrhagic fever cases. The only means of transportation betweenthese two areas is by boat; Makokou, the closest town to them (Figure3), has the provincial hospital to which patients and contacts weretransferred. The third outbreak, started in July 1996 in the village ofBoou (Figure 3), where most of the cases occurred; however, scatteredcases have been diagnosed in surrounding villages and towns. Somepatients have even been transported to Libreville, probably during theincubation period of the disease. One patient was treated in SouthAfrica, where a fatal nosocomial infection was subsequently reported ina health care worker; over 43 deaths due to Ebola hemorrhagic feverwere reported during this prolonged outbreak. There were many genesequences obtained from human samples during each of the three Gaboneseepidemics. Some was obtained from blood collected 1 day before thedeath of a patient, from the Nouna area, during the 1994 outbreak.Other sequences were derived from blood collected during the spring1996 outbreak, from two primary patients who were infected whilebutchering a chimpanzee they found dead in the forest. One sequence wasderived from blood collected from what appears to have been a secondarycase during the same outbreak; the patient was probably infected bycontact with one of the index patients while visiting a traditionaldoctor who lived near Mayibout village. The isolation of Ebola virusin a cell culture from human blood samples collected during the threedifferent outbreaks was easily accomplished in a single passage. RNAwas extracted from blood or primary tissue culture samples by using acommercial kit. Viral sequences were amplified from RNA by using thereverse transcriptase-polymerase chain reaction technique. Briefly,amplified products were subjected to agarose electrophoresis and werestained and visualized with ethidium bromide; DNA bands were thenexcised and extracted. In some cases, nested PCR with internal primerswas performed, using first-round products. Amplified products weredirectly sequenced by using an automated nonisotopic method. Excessdye-labeled dideoxynucleotide terminators were removed, and reactionproducts were analyzed. A consensus sequence was established byaligning all the Ebola from Gabon, the Zaire 1976 and 1995 Ebola virussequences, as well as the sequence of the virus obtained from a nursein South Africa who was infected of the three different outbreaks in Gabon. Although the viruses causing the Gabonese outbreaks clearly belong to the Zaire subtype, they were distinct from viruses that had caused disease in Zaire. No differences were observed between tissue-culture-passaged and clinical-material-derived sequences or between primary or secondary case sequences. RNA extracted from a single representative of each outbreak was then used to generate the entire gene sequence for the Gabon Ebola viruses. The gene sequence from the Gabon spring 1996 viruses differed from the sequence of the Gabon fall 1994 viruses by four nucleotides. The genetic sequence from the Gabon fall 1996 viruses differed from the sequence of the Gabon spring 1996 virus by four additional nucleotides. A single most parsimonious tree wasobtained (Figure 4), and bootstrap analysis strongly supports a commonevolutionary origin for the viruses associated with disease in Gabonand Zaire. Overall, these data indicate that the three Gabon outbreaksshould be considered independent events, likely originating fromdifferent sources. The presence of stable virus sequences and the lackof genetic variability between strains isolated within an outbreak waspreviously seen during the outbreak of Ebola hemorrhagic fever inKikwit, Zaire, in 1995, and despite the small number of isolatestested, is again suggested in Gabon. During a 20-month period, Gabonhad three different outbreaks of Ebola virus hemorrhagic fever. Thefirst and the second episodes apparently started during the rainyseason (December and February), while the third began during the dryseason (July). The deaths of nonhuman primates were associated with allthree outbreaks. Minkouka area inhabitants reported finding deadchimpanzees and gorillas in the forest during the fall of 1994. All theprimary human patients in the spring 1996 outbreak were infected whilebutchering dead chimpanzees. For the third outbreak, the investigationhas indicated an index patient who was a hunter, living in a forestcamp in the Boou area. During the same period, an Ebola virus-infecteddead ch In Cte d’Ivoire in 1994, an investigator was infected withEbola virus while performing necropsy on a dead chimpanzee. Primatesare unlikely to be the reservoir of Ebola virus since experimental ornatural infection is quickly fatal. A better knowledge of the ecologyof great apes, particularly their food preferences and habitats, maylead to the identification of the virus reservoir. Gabon’s equatorialforests, where three independent outbreaks have occurred in less than 3years, offer an excellent opportunity for these investigations. It hasnow become apparent that the only solution to this problem, whichsociety is increasingly becoming aware of, is diligent research andexperimentation. The CDC continues to inject infant mice and guineapigs with the virus and document the details of either their deaths orrecoveries. It is the hopes of both the scientific community and therest of the world that some tangible solution be found as soon aspossible. Figure 1. Spikes surrounding the virus. Figure 2. The “U” Shape of the virus. Figure 3. Geographic distribution of the three Ebola virushemorrhagic fever epidemics and site of the infectedchimpanzee in Gabon. Figure 4. Phylogenetic tree showing the relationshipbetween the Ebola viruses that caused outbreaks of diseasein Gabon and previously described filoviruses. Theentire coding region for the glycoprotein gene of the virusesshown was used in maximum parsimony analysis, and asingle most parsimonious tree was obtained. Numbers inparentheses indicate bootstrap confidence values for branch points and were generated from 500 replicatesBranch length values are also shown. Figure 5. Immunostaining of Ebola virus antigens (red) within vascularendothelial cells in skin biopsy of the chimpanzee found dead in theforest near Boou. Note also the presence of extracellular viralantigens. Bibliography bjach.polk.amedd.army.mil/B8/Ebola.htm. Ebola galaxy.einet.net/galaxy/medicine/Diseases-and-Disorders/Viruses-Diseases/RNA-Virus-I infections/Ebola-Hemorrhagic-Fever.html. RNA Virus Infections Microsoft Encarta Encyclopedia 97 Ebola Star and Taggart. Biology: The Unity and Diversity of Life. Wadsworth. Toronto.1998 www.bocklabs.wisc.edu. Marburg and Ebola Viruses www.cdc.gov. Centers for Disease Control and Prevention. February 5, 1997 www.infowire.vet/brett/personal/eframe.html Ebola Page www.outbreak.com. The Outbreak Page Essay Data SectionEbola VirusType: Student Submitted || Return To The Student Essay Directory ||

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