Ebola virus
E•bo′la vi`rus
(ɪˈboʊ lə)n.
E·bo·la virus
(ĭ-bō′lə)| Noun | 1. | Ebola virus - a filovirus that causes Ebola hemorrhagic fever; carried by animals; can be used as a bioweapon |
n.
Ebola virus
Ebola virus
(ēbō`lə), a virus of the genus Ebolavirus, which belongs to a family (Filoviridae) of RNA virusesvirus,parasite with a noncellular structure composed mainly of nucleic acid within a protein coat. Most viruses are too small (100–2,000 Angstrom units) to be seen with the light microscope and thus must be studied by electron microscopes.
..... Click the link for more information. that cause hemorrhagic fevers. The viruses, named for the region in Congo (Kinshasa) where the first species was first identified in 1976, emerged from the rain forest, where they survive in as yet unconfirmed hosts, possibly several species of fruit bats (one Ebolavirus species has been found in some fruit bats) but potentially other mammal species; experimental evidence suggests that wild and domestic swine may be a reservoir of the disease. The virus can be fatal to chimpanzees and gorillas as well as humans.
Several species of Ebolavirus found in Africa cause Ebola virus disease (formerly known as Ebola hemorrhagic fever); one found in the W Pacific, which was first identified (1989) in monkeys imported into the United States, does not. Once a person is infected, the disease has an incubation period of 2–21 days; however, some infected persons are asymptomatic. Initial symptoms are sudden malaise, headache, and muscle pain, progressing to high fever, diarrhea, vomiting, symptoms of kidney and liver impairment, and in some cases severe hemorrhaging (internally and out of the eyes and mouth). In 25%–90% of patients, death results, usually within days. The virus is transmitted in body fluids and secretions; it may possibly also be transmitted through the air by aerosol droplets. There is no cure. A vaccine, rVSV-ZEBOV, has been developed against the species that caused the 2013–15 West African outbreak. It was effective, but it was experimental and saw limited use during the outbreak. It is unclear if the protection provided by the vaccine will be long lasting.
Outbreaks of Ebola virus in humans have typically occurred in tropical rainforest regions in Central and West Africa. Among the countries affected have been Congo-Kinshasa (then Zaïre) and Sudan (in a region now in South Sudan), where outbreaks occurred in 1976 and 1979; since then other outbreaks have occurred in Gabon, Uganda, and both Congos. The largest and deadliest outbreak began in late 2013 in Guinea and spread to neighboring Liberia and Sierra Leone, with a few cases in some nearby African nations and in the United States and Europe; some 11,300 people—many more than in any prior outbreak—died in the following two years. Outbreaks have been exacerbated by underequipped and understaffed medical facilities, families caring for patients at home, suspicions that medical personnel are spreading the disease, and other factors.
Bibliography
See D. Quammen, Ebola (2014).
Ebola virus
Ebola viruses are a group of exotic viral agents that cause a severe hemorrhagic fever disease in humans and other primates. The four known subtypes or species of Ebola viruses are Zaire, Sudan, Reston, and Côte d'Ivoire (Ivory Coast), named for the geographic locations where these viruses were first determined to cause outbreaks of disease. Ebola viruses are very closely related to, but distinct from, Marburg viruses. Collectively, these pathogenic agents make up a family of viruses known as the Filoviridae.
Filoviruses have an unusual morphology, with the virus particle, or virion, appearing as long thin rods. A filovirus virion is composed of a single species of ribonucleic acid (RNA) molecule that is bound together with special viral proteins, and this RNA–protein complex is surrounded by a membrane derived from the outer membrane of infected cells. Infectious virions are formed when the virus buds from the surface of infected cells and is released. Spiked structures on the surface of virions project from the virion and serve to recognize and attach to specific receptor molecules on the surface of susceptible cells, allowing the virion to penetrate the cell. The genetic information contained in the RNA molecule directs production of new virus particles by using the cellular machinery to drive synthesis of new viral proteins and RNA. See Ribonucleic acid (RNA), Virus
Although much is known about the agents of Ebola hemorrhagic fever disease, the ecology of Ebola viruses remains a mystery. The natural hosts of filoviruses remain unknown, and there has been little progress at unraveling the events leading to outbreaks or identifying sources of filoviruses in the wild. Fortunately, the incidence of human disease is relatively rare and has been limited to persons living in equatorial Africa or working with the infectious viruses. The virus is spread primarily through close contact with the body of an infected individual, his or her body fluids, or some other source of infectious material.
Ebola virus hemorrhagic fever disease in humans begins with an incubation period of 4–10 days, which is followed by abrupt onset of illness. Fever, headache, weakness, and other flulike symptoms lead to a rapid deterioration in the condition of the individual. In severe cases, bleeding and the appearance of small red spots or rashes over the body indicate that the disease has affected the integrity of the circulatory system. Individuals with Ebola virus die as a result of a shock syndrome that usually occurs 6–9 days after the onset of symptoms. This shock is due to the inability to control vascular functions and the massive injury to body tissues.
It appears that the immune response is impaired and that a strong cellular immune response is key to surviving infections. This immunosuppression may also be a factor in death, especially if secondary infections by normal bacterial flora ensue. See Immunosuppression
Outbreaks of Ebola virus disease in humans are controlled by the identification and isolation of infected individuals, implementation of barrier nursing techniques, and rapid disinfection of contaminated material. Diagnosis of Ebola virus cases is made by detecting virus proteins or RNA in blood or tissue specimens, or by detecting antibodies to the virus in the blood.
Dilute hypochlorite solutions (bleach), 3% phenolic solutions, or simple detergents (laundry or dish soap) can be used to destroy infectious virions. No known drugs have been shown to be effective in treating Ebola virus (or Marburg virus) infections, and protective vaccines against filoviruses have not been developed.
Ebola virus
virus
[vi´rus]Unlike cellular organisms, viruses do not contain all the biochemical mechanisms for their own replication; they replicate by using the biochemical mechanisms of a host cell to synthesize and assemble their separate components. (Some do contain or produce essential enzymes when there is no cellular enzyme that will serve.) When a complete virus particle (virion) comes in contact with a host cell, only the viral nucleic acid and, in some viruses, a few enzymes are injected into the host cell.
Within the host cell the genetic material of a DNA virus is replicated and transcribed into messenger RNA by host cell enzymes, and proteins coded for by viral genes are synthesized by host cell ribosomes. These are the proteins that form the capsid (protein coat); there may also be a few enzymes or regulatory proteins involved in assembling the capsid around newly synthesized viral nucleic acid, in controlling the biochemical mechanisms of the host cell, and in lysing the host cell when new virions have been assembled. Some of these may already have been present within the initial virus, and others may be coded for by the viral genome for production within the host cell.
Because host cells do not have the ability to replicate “viral RNA” but are able to transcribe messenger RNA, RNA viruses must contain enzymes to produce genetic material for new virions. For certain viruses the RNA is replicated by a viral enzyme (transcriptase) contained in the virion, or produced by the host cell using the viral RNA as a messenger. In other viruses a reverse transcriptase contained in the virion transcribes the genetic message on the viral RNA into DNA, which is then replicated by the host cell. Reverse transcriptase is actually a combination of two enzymes: a polymerase that assembles the new DNA copy and an RNase that degrades the source RNA.
In viruses that have membranes, membrane-bound viral proteins are synthesized by the host cell and move, like host cell membrane proteins, to the cell surface. When these proteins assemble to form the capsid, part of the host cell membrane is pinched off to form the envelope of the virion.
Some viruses have only a few genes coding for capsid proteins. Other more complex ones may have a few hundred genes. But no virus has the thousands of genes required by even the simplest cells. Although in general viruses “steal” their lipid envelope from the host cell, virtually all of them produce “envelope proteins” that penetrate the envelope and serve as receptors. Some envelope proteins facilitate viral entry into the cell, and others have directly pathogenic effects.
Some viruses do not produce rapid lysis of host cells, but rather remain latent for long periods in the host before the appearance of clinical symptoms. This carrier state can take any of several different forms. The term latency is used to denote the interval from infection to clinical manifestations. In the lentiviruses, it was formerly mistakenly believed that virus was inactive during this period. The true situation is that lentiviruses are rapidly replicating and spawning dozens of quasi-species until a particularly effective one overruns the ability of the host's immune system to defeat it. Other viruses, however, such as the herpesviruses, actually enter a time known as “viral latency,” when little or no replication is taking place until further replication is initiated by a specific trigger. For many years all forms of latency were thought to be identical, but now it has been discovered that there are different types with basic and important distinctions.
In viral latency, most of the host cells may be protected from infection by immune mechanisms involving antibodies to the viral particles or interferon. Cell-mediated immunity is essential, especially in dealing with infected host cells. Cytotoxic lymphocytes may also act as antigen-presenting cells to better coordinate the immune response. Containment of virus in mucosal tissues is far more complex, involving follicular dendritic cells and Langerhans cells.
Some enveloped RNA viruses can be produced in infected cells that continue growing and dividing without being killed. This probably involves some sort of intracellular regulation of viral growth. It is also possible for the DNA of some viruses to be incorporated into the host cell DNA, producing a carrier state. These are almost always retroviruses, which are called proviruses before and after integration of viral DNA into the host genome.
Few viruses produce toxins, although viral infections of bacteria can cause previously innocuous bacteria to become much more pathogenic and toxic. Other viral proteins, such as some of the virus" >human immunodeficiency virus, appear to be actively toxic, but those are the exception, not the rule.
However, viruses are highly antigenic. Mechanisms of pathologic injury to cells include cell lysis; induction of cell proliferation (as in certain warts and molluscum contagiosum); formation of giant cells, syncytia, or intracellular inclusion bodies caused by the virus; and perhaps most importantly, symptoms caused by the host's immune response, such as inflammation or the deposition of antigen-antibody complexes in tissues.
Because viral reproduction is almost completely carried out by host cell mechanisms, there are few points in the process where stopping viral reproduction will not also kill host cells. For this reason there are no chemotherapeutic agents for most viral diseases. acyclovir is an antiviral that requires viral proteins to become active. Some viral infections can be prevented by vaccination (immunization" >active immunization), and others can be treated by immunization" >passive immunization with globulin" >immune globulin, although this has been shown to be effective against only a few dozen viruses.
E·bo·la vi·rus
(ēb'ō-lă),Vector Unknown, probably fruit and insectivorous bats
Serotypes Ebola Zaire, E Sudan, E Reston
Management Supportive
Military medicine EV has potential as a biological weapon; the Ebola-Zaire virus was responsible for an outbreak in Gabon in which there were 37 confirmed persons with Ebola hemorrhagic fever, of whom 21 died; the Gabon outbreak was linked to the butchering, transport and preparation for consumption of a chimpanzee found dead in the forest
E·bo·la vi·rus
(ē-bō'lă vī'rŭs)Ebola virus
an animal virus that can kill humans and other primates (apes and monkeys). It causes severe haemorrhaging and death occurs within one or two weeks. The virus has been responsible for serious EPIDEMICS of disease in humans, such as the outbreaks in regions of Africa in 1976 and 1995, and no vaccine is presently available. It appears that there are other HOSTS that can maintain the virus but are not killed by it. Ebola is a filovirus (filo- meaning ‘threadlike’, reflecting its morphology) and it has an RNA GENOME. The only other known filovirus is Marburg virus.Ebola,
river in Zaire, Africa.Patient discussion about Ebola virus
Q. Ebola is serious I heard that Ebola is serious disease crapping out the inner lining of our intestines, the lining of our tongue peeling off, blood comming out of every hole in our body, including our nips. not too much fun. Could anyone tell me about the treatment for this. So this can educate me and other who read this.
See EBOV
Ebola virus
- noun
Words related to Ebola virus
noun a filovirus that causes Ebola hemorrhagic fever
Related Words
- Filoviridae
- filovirus
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