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Ebola virus

Article by: Sanchez, Anthony Department of Health and Human Services, Centers for Disease Control and Prevention, Atlanta, Georgia. Publication year: 2014 DOI: http://dx.doi.org/10.1036/1097-8542.757464 (http://dx.doi.org/10.1036/1097-8542.757464)

Content

• Infectious agent • Pathogenesis • Diagnosis • Epidemiology • Control and prevention •Evolution • Bibliography • Additional Readings

Ebola 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, viruses. Collectively, these pathogenic agents make up a family of viruses known as the .

Infectious agent

Filoviruses have an unusual morphology, with the virus particle, or virion, appearing as long thin rods. Virions have a diameter of 0.08 micrometer and a minimal length of 0.7–0.9 μm; this length is comparable to that of a small bacterium. However, when these viruses are grown in cell cultures, they can form long filamentous and branched forms that reach 14 μm or more. This is especially true for Ebola viruses.

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 are formed by three molecules of a single glycoprotein and are firmly embedded in the virion membrane. These structures project from the virion and serve to recognize and attach to specific receptor molecules on the surface of susceptible cells. This recognition and binding allows the virion to penetrate into the cell. Then, with the virion free to operate within

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the cytoplasm, 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 also: Ribonucleic acid (RNA) (/content/ribonucleic-acid-rna/589000); Virus (/content/virus/733500)

Pathogenesis

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. However, in this time of rapid transportation over large distances, the threat of agents such as Ebola viruses spreading to remote areas is taken very seriously by public health professionals. People infected with the virus are not as contagious as, say, persons suffering from a cold or measles, and 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.

Diagnosis

Ebola virus hemorrhagic fever disease in humans begins with an 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. Contrary to popular belief, individuals with Ebola virus infections do not melt or have their organs dissolve, but 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.

Ebola viruses can be found in high concentrations in tissues throughout the body and are especially evident in the liver, spleen, and skin. From studies of human cases and experimentally infected animals, 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. No severe human disease has been associated with infections, and it appears that this virus may be much less pathogenic for humans than it is for monkeys. See also: Immunosuppression (/content/immunosuppression/338950)

Epidemiology

The first described cases of Ebola virus disease occurred in 1976, when simultaneous outbreaks of two distinct subtypes occurred in northern Zaire and southern Sudan. Many of the human infections occurred in local hospitals, where close contact with fatal cases, reuse of contaminated needles, and a low standard of medical care led to most fatalities. An Asian form of Ebola virus was discovered in a type of macaque, the cynomolgus, exported from the to the United States in late 1989. It was determined that a single monkey breeding facility in the Philippines was the source of the virus. Named Reston virus after the

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city in which infected monkeys were first identified, it represented a new form of Ebola virus. A repeat of this incident took place in early 1992, when monkeys from the same breeding facility were shipped to Siena, Italy.

In 1994, another new species of Ebola virus was identified, associated with chimpanzee deaths in the west African country of Côte d'Ivoire. This episode signaled the reemergence of Ebola virus in Africa, which had not been seen since 1979 when an outbreak of the Sudan subtype occurred. A large outbreak of disease was identified in early May 1995 in and around the city of Kikwit, Zaire. This outbreak of a Zaire subtype was a repeat of the 1976 episode, but this time 600 mi (1000 km) to the south. Another Ebola virus outbreak took place in 1995 in Gabon and resulted in human fatalities, but the details were slow to be revealed. This virus has been isolated, and preliminary reports indicate that it may be a variant of the Zaire subtype. This virus may have also been responsible for human fatalities in Gabon reported to have occurred in early 1996. Soon after this outbreak, yet another Reston virus outbreak occurred when infected monkeys were sent to a United States holding facility in Alice, . That introduction was quickly detected and stopped by quarantine and testing measures implemented after the first Reston virus episode in 1989.

Control and prevention

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 to the virus in the blood. Such testing is important in tracking and controlling the movement of the virus during an outbreak.

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 ) infections, and protective vaccines against filoviruses have not been developed. However, research is being directed at developing such treatment and should provide insights into the disease mechanisms used by filoviruses.

Evolution

Filoviruses have been shown to be genetically related to two other virus families, the (including measles virus and mumps virus) and the (including virus and vesicular stomatitis virus). These viruses evolved from a common progenitor in the very distant past. These viruses evolved into very distinct lineages, yet have maintained a similar approach to reproducing.

The evolutionary profile, or phylogeny, for Ebola viruses and Marburg viruses has been determined. Ebola viruses have evolved into a separate and very distinct lineage within the filovirus family, and the individual species of Ebola viruses have also evolved into their own sublineages. Filoviruses show a great deal of diversity, indicating that they have likely coevolved with their natural hosts over a long period of time. Ebola

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viruses within a given subtype did not appear to show a great deal of change over periods of many years. This genetic stability or stasis in the wild suggests that these viruses have evolved to occupy very specific ecological niches.

Anthony Sanchez

Bibliography

Centers for Disease Control, Ebola-Reston virus infection among quarantined nonhuman primates—Texas, 1996, MMWR, 45:314–316, 1996

D. M. Knipe et al. (eds.), Fields Virology, 5th ed., 2007

L. G. Horowitz, Emerging Viruses: AIDS and Ebola—Nature, Accident or Intentional, 1996

A. Sanchez et al., Reemergence of Ebola virus in Africa, Emerg. Infect. Dis., 1:96–97, 1995 DOI: 10.3201/eid0103.950307 (http://dx.doi.org/10.3201/eid0103.950307)

A. Sanchez et al., The virion glycoproteins of Ebola viruses are encoded in two reading frames and are expressed through transcriptional editing, Proc. Natl. Acad. Sci. USA, 93:3602–3607, 1996 DOI: 10.1073/pnas.93.8.3602 (http://dx.doi.org/10.1073/pnas.93.8.3602)

Additional Readings

L. A. Beltz, Emerging Infectious Diseases: A Guide to Diseases, Causative Agents, and Surveillance, John Wiley & Sons, San Francisco, CA, 2011

M. García et al., Productive replication of Ebola virus is regulated by the c-Abl1 tyrosine kinase, Sci. Transl. Med., 4(123):123ra24–123ra24, 2012 DOI: 10.1126/scitranslmed.3003500 (http://dx.doi.org/10.1126/scitranslmed.3003500)

T. Shoemaker et al., Reemerging Sudan Ebola virus disease in Uganda, Emerg. Infect. Dis., 18(9):1480, 2012 DOI: 10.3201/eid1809.111536 (http://dx.doi.org/10.3201/eid1809.111536)

C. Tidona and G. Darai (eds.), The Springer Index of Viruses, 2d ed., Springer, New York, 2011

C. Zimmer, A Planet of Viruses, The University of Chicago Press, Chicago, IL, 2011

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