Causes EVD is caused by four of five viruses classified in the genus Ebolavirus, family Filoviridae, order Mononegavirales. The four disease-causing viruses are Bundibugyo virus (BDBV), Sudan virus (SUDV), Taï Forest virus (TAFV), and one called simply, Ebola virus (EBOV, formerly Zaire Ebola virus)). Ebola virus is the sole member of the Zaire ebolavirus species, and the most dangerous of the known Ebola disease-causing viruses, as well as being responsible for the largest number of outbreaks.[16] The fifth virus, Reston virus (RESTV), is not thought to be disease-causing in humans. The five Ebola viruses are closely related to the Marburg viruses. Transmission It is not entirely clear how Ebola is spread. EVD is believed to occur after an ebola virus is transmitted to an initial human by contact with an infected animals body fluids. Human-to-human transmission can occur via direct contact with blood or bodily fluids from an infected person (including embalming of an infected dead person) or by contact with contaminated medical equipment, particularly needles and syringes. The potential for widespread EVD infections is considered low as the disease is only spread by direct contact with the secretions from someone who is showing signs of infection. The quick onset of symptoms makes it easier to identify sick individuals and limits a persons ability to spread the disease by traveling. Because dead bodies are still infectious local traditional burial rituals may spread the disease. Semen may be infectious in survivors for up to 50 days. Medical workers who do not wear appropriate protective clothing may also contract the disease. In the past, hospital-acquired transmission has occurred in African hospitals due to the reuse of needles and lack of universal precautions. Airborne transmission has not been documented during EVD outbreaks. They are, however, infectious as breathable 0.8– to 1.2-μm laboratory-generated droplets. The virus has been shown to travel without contact from pigs to nonhuman primates, although the same study failed to achieve transmission in that manner between primates. Bats drop partially eaten fruits and pulp, then land mammals such as gorillas and duikers feed on these fallen fruits. This chain of events forms a possible indirect means of transmission from the natural host to animal populations, which has led to research towards viral shedding in the saliva of bats. Fruit production, animal behavior, and other factors vary at different times and places that may trigger outbreaks among animal populations. Reservoir Bushmeat being prepared for cooking in Ghana, 2013 Human consumption of equatorial animals in Africa in the form of bushmeat has been linked to the transmission of diseases to people, including Ebola. Bats are considered the most likely natural reservoir of the EBOV; plants, arthropods, and birds have also been considered. Bats were known to reside in the cotton factory in which the first cases for the 1976 and 1979 outbreaks were employed, and they have also been implicated in Marburg virus infections in 1975 and 1980. Of 24 plant species and 19 vertebrate species experimentally inoculated with EBOV, only bats became infected. The absence of clinical signs in these bats is characteristic of a reservoir species. In a 2002–2003 survey of 1,030 animals including 679 bats from Gabon and the Republic of the Congo, 13 fruit bats were found to contain EBOV RNA fragments. As of 2005, three types of fruit bats (Hypsignathus monstrosus, Epomops franqueti, and Myonycteris torquata) have been identified as being in contact with EBOV. They are now suspected to represent the EBOV reservoir hosts. Antibodies against Ebola Zaire and Reston viruses have been found in fruit bats in Bangladesh, thus identifying potential virus hosts and signs of the filoviruses in Asia. Between 1976 and 1998, in 30,000 mammals, birds, reptiles, amphibians and arthropods sampled from outbreak regions, no ebolavirus was detected apart from some genetic traces found in six rodents (Mus setulosus and Praomys) and one shrew (Sylvisorex ollula) collected from the Central African Republic. Traces of EBOV were detected in the carcasses of gorillas and chimpanzees during outbreaks in 2001 and 2003, which later became the source of human infections. However, the high lethality from infection in these species makes them unlikely as a natural reservoir.[28] Transmission between natural reservoir and humans is rare, and outbreaks are usually traceable to a single case where an individual has handled the carcass of gorilla, chimpanzee or duiker.Fruit bats are also eaten by people in parts of West Africa where they are smoked, grilled or made into a spicy soup. Virology Electron micrograph of an Ebola virus virion Like all mononegaviruses, ebolavirions contain linear nonsegmented, single-strand, non-infectious RNA genomes of negative polarity that possesses inverse-complementary 3 and 5 termini, do not possess a 5 cap, are not polyadenylated, and are not covalently linked to a protein. Ebolavirus genomes are approximately 19 kilobase pairs long and contain seven genes in the order 3-UTR-NP-VP35-VP40-GP-VP30-VP24-L-5-UTR.[38] The genomes of the five different ebolaviruses (BDBV, EBOV, RESTV, SUDV, and TAFV) differ in sequence and the number and location of gene overlaps. Structure Like all filoviruses, ebolavirions are filamentous particles that may appear in the shape of a shepherds crook or in the shape of a U or a 6, and they may be coiled, toroid, or branched. In general, ebolavirions are 80 nm in width, but vary somewhat in length. In general, the median particle length of ebolaviruses ranges from 974 to 1,086 nm (in contrast to marburgvirions, whose median particle length was measured at 795–828 nm), but particles as long as 14,000 nm have been detected in tissue culture. Replication The ebolavirus life cycle begins with virion attachment to specific cell-surface receptors, followed by fusion of the virion envelope with cellular membranes and the concomitant release of the virus nucleocapsid into the cytosol. The viral RNA polymerase, encoded by the L gene, partially uncoats the nucleocapsid and transcribes the genes into positive-strand mRNAs, which are then translated into structural and nonstructural proteins. Ebolavirus RNA polymerase (L) binds to a single promoter located at the 3 end of the genome. Transcription either terminates after a gene or continues to the next gene downstream. This means that genes close to the 3 end of the genome are transcribed in the greatest abundance, whereas those toward the 5 end are least likely to be transcribed. The gene order is, therefore, a simple but effective form of transcriptional regulation. The most abundant protein produced is the nucleoprotein, whose concentration in the cell determines when L switches from gene transcription to genome replication. Replication results in full-length, positive-strand antigenomes that are, in turn, transcribed into negative-strand virus progeny genome copy. Newly synthesized structural proteins and genomes self-assemble and accumulate near the inside of the cell membrane. Virions bud off from the cell, gaining their envelopes from the cellular membrane they bud from. The mature progeny particles then infect other cells to repeat the cycle.The Ebola Virus genetics are difficult to study due to its virulent nature
Posted on: Thu, 09 Oct 2014 18:54:53 +0000
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