Ok with all these uneducated conspiracies floating around about the Ebola virus. Please stop reposting bull shit thats not even true. Here are some facts for you. The known members of the family Filoviridae are the genera Ebolavirus (Ebola virus) and Marburgvirus (Marburg virus). According the 2012 virus taxonomy of the International Committee on Taxonomy of Viruses, Ebolavirus is classified into the following 5 separate species: Sudan ebolavirus Zaire ebolavirus Tai Forest ebolavirus (formerly and perhaps still more commonly Ivory Coast ebolavirus or Côte d’Ivoire ebolavirus) Reston ebolavirus Bundibugyo ebolavirus Filoviruses such as Ebola virus share a characteristic filamentous form, with a uniform diameter of approximately 80 nm but a highly variable length. Filaments may be straight, but they are often folded on themselves. a virus has a nonsegmented negative-stranded RNA genome containing 7 structural and regulatory genes. The Ebola genome codes for 4 virion structural proteins (VP30, VP35, nucleoprotein, and a polymerase protein [L]) and 3 membrane-associated proteins (VP40, glycoprotein [GP], and VP24). The GP gene is positioned fourth from the 3′ end of the 7 linearly arranged genes. After infection, human and nonhuman primates experience an early period of rapid viral multiplication that, in lethal cases, is associated with an ineffective immunologic response. Although a full understanding of Ebola virus disease must await further investigations, part of the pathogenesis has been elucidated. Most filovirus proteins are encoded in single reading frames; the surface GP is encoded in 2 frames (open reading frame [ORF] I and ORF II). The ORF I (amino-terminal) of the gene encodes for a small (50-70 kd), soluble, nonstructural secretory glycoprotein (sGP) that is produced in large quantities early in Ebola virus infection.[4] The sGP binds to neutrophil CD16b, a neutrophil-specific Fc g receptor III, and inhibits early neutrophil activation. The sGP also may be responsible for the profound lymphopenia that characterizes Ebola infection. Thus, sGP is believed to play pivotal roles in the ability of Ebola to prevent an early and effective host immune response. One hypothesis is that the lack of sGP production by Marburg virus may explain why this agent is less virulent than African-derived Ebola virus. Leroy et al reported their observations of 24 close contacts of symptomatic patients actively infected with Ebola.[5] Eleven of the 24 contacts developed evidence of asymptomatic infection associated with viral replication. Viral replication was proven by the authors’ ability to amplify positive-stranded Ebola virus RNA from the blood of the asymptomatic contacts. A detailed study of these infected but asymptomatic individuals revealed that they had an early (4-6 days after infection) and vigorous immunologic response with production of interleukin (IL)–1β, IL-6, and tumor necrosis factor (TNF), resulting in enhanced cell-mediated and humoral-mediated immunity. In patients who eventually died, proinflammatory cytokines were not detected even after 2-3 days of symptomatic infection. A second, somewhat larger (120-150 kd) GP, transmembrane glycoprotein, is incorporated into the Ebola virion and binds to endothelial cells but not to neutrophils. Ebola virus is known to invade, replicate in, and destroy endothelial cells. Destruction of endothelial surfaces is associated with disseminated intravascular coagulation, and this may contribute to the hemorrhagic manifestations that characterize many, but not all, Ebola infections. Clinical infection in human and nonhuman primates is associated with rapid and extensive viral replication in all tissues. Viral replication is accompanied by widespread and severe focal necrosis. The most severe necrosis occurs in the liver, and this is associated with the formation of Councilman-like bodies similar to those seen in yellow fever. In fatal infections, the host’s tissues and blood contain large numbers of Ebola virions, and the tissues and body fluids are highly infectious. The 5 Ebolavirus species were named for the locations where they caused documented human or animal disease. Two African species, Sudan ebolavirus and Zaire ebolavirus, have been responsible for most of the reported deaths. Clinical disease due to African-derived Ebola virus is severe and, with the exception of a patient who survived infection with a third African species, Ivory Coast ebolavirus, is associated with a mortality ranging from 65% (Sudan, 1979) to 89% (Democratic Republic of the Congo [DRC], December 2002 to April 2003). A fourth Ebolavirus species, Reston ebolavirus, was first isolated in 1989 in monkeys imported from a single Philippine exporter. A virtually identical isolate imported from the same Philippine exporter was detected in 1992 in Siena, Italy. To date, this species has not been documented to cause human disease. The fifth Ebolavirus species, also of African lineage, is Bundibugyo ebolavirus, which caused an outbreak in Uganda in 2007-2008, with a mortality of 25%.[6] Between 1994 and 1997, a stable strain of Ebola virus caused 3 successive outbreaks of hemorrhagic fever in Gabon (mortality, 60-74%).[7] Because the Gabon strain shares a greater than 99% homology of the nucleoprotein and GP gene regions with Zaire ebolavirus, it has not been considered a distinct species. A likely reservoir for filoviruses has been identified. In 1996, members of the National Institute for Virology of South Africa went to Kikwit, DRC, and evaluated the infectivity of Ebola virus for 24 species of plants and 19 species of vertebrates and invertebrates.[8] Insectivorous bats and fruit bats were found to support Ebola virus replication without dying. Furthermore, serum Ebola titers in infected fruit bats reached as high as 106 fluorescent focus-forming units/mL, and feces contained viable Ebola virus. Mechanisms of dispersion African-derived filovirus infections are characterized by transmission from an unknown host (possibly bats) to humans or nonhuman primates, presumably via direct contact with body fluids such as saliva or blood or other infected tissues. Evidence in nonhuman primates indicates that Sudan ebolavirus and Zaire ebolavirus may be transmitted by contact with mucous membranes, conjunctiva, pharyngeal and gastrointestinal (GI) surfaces; through small breaks in the skin; and, at least experimentally, by aerosol.[9] Dogs have been shown to acquire asymptomatic Ebola virus infections, possibly by contact with virus-laden droplets of urine, feces, or blood of unknown hosts.[10] Of epidemiologic significance was the observation that seroprevalence rates in dogs rose in a linear fashion as sampling approached areas of human cases, reaching as high as 31.8%. Thus, an increase in canine seroprevalence may serve as an indicator of increasing Ebola virus circulation in primary vectors within specific geographical areas. Human infection with African-derived strains has often occurred in caregivers (either family or medical) and in family members who have prepared dead relatives for burial. Late stages of Ebola virus disease are associated with the presence of large numbers of virions in body fluids, tissues, and, especially, skin. Individuals who are exposed to patients infected with Ebola without proper barrier protection are at high risk of becoming infected. A report from the DRC identified Ebola virus RNA in 100% of oral secretions from patients who had the viral RNA in their serum. Both serum and oral secretions were tested with reverse-transcriptase polymerase chain reaction (RT-PCR) assay. Thus, oral secretions may be capable of transmitting Ebola virus. The first recorded outbreak occurred in 1976, in Yambuku, DRC, where 316 patients were infected. In the largest recorded urban outbreak to date (DRC, 1995; 318 cases), admission to a hospital greatly amplified the frequency of transmission. The lack of proper barrier protection and the use and reuse of contaminated medical equipment, especially needles and syringes, resulted in rapid nosocomial spread of infection. Only after adequate barrier protection and alteration in burial rituals were implemented was the outbreak contained. Unlike Asian-derived Ebola virus (ie, Reston ebolavirus, traced to a Philippine supplier of primates), African-derived species appear to be spread more often by direct contact than via the respiratory route. However, the Reston species has repeatedly been demonstrated to spread among nonhuman primates and possibly from primates to humans via the respiratory route. Fortunately, although the Reston species has been documented to be capable of infecting in humans, it does not appear to be pathogenic to humans. With the research out the way more facts. The virus has not been airborne outside of a very specific conditions that made it possible and shortly effective at that. The viruses first recorded as an outbreak and identified as those particular viruses in 1976. It was not manufactured in some lab. It is speculated that the great plagues in the Bible may have been indeed re Ebola virus which would means it was before laboratories even existed. There was no one that died then came back to life. The zombie Ebola carrying people were never dead. Also never been embalmed. The phrase dead ringer pays tribute to that fact. The person heart may stop beating and they might stop breathing but the brain isnt dead. Neurons fire long after the body stops functioning. Your brain can fire electrons to make your heart beat and you to take a breath to start back living (recorded as long as 3 days later. Slight brain damage may be a result which will give them the sluggish zombie effect. But they didnt come back from the dead. It was a delayed response from their body plus we dont know the credentials of those whom pronounced them dead. If they had a fear of contracting the disease Im sure they didnt check that close. Yes the virus can mutate. Any virus can. Its not likely to become airborne. It is contracted through physically coming in contact with the virus. So bodily fluids containing it mostly blood and vomit. Cured males can pass the virus up to 2 months after being cured in semen. To diagnose Ebola they must rule out diseases with similar symptoms such as malaria, cholera and other viral hemorrhagic fevers are first excluded. To confirm the diagnosis, blood samples are tested for viral antibodies, viral RNA, or the virus itself. Prevention includes decreasing the spread of disease from infected animals to humans. This may be done by checking such animals for infection and killing and properly disposing of the bodies if the disease is discovered. Properly cooking meat and wearing protective clothing when handling meat may also be helpful, as are wearing protective clothing and washing hands when around a person with the disease. Samples of bodily fluids and tissues from people with the disease should be handled with special caution.
Posted on: Sat, 04 Oct 2014 00:15:44 +0000