Ebola Virus

Ebola Virus Ebola virus, a member of the Filoviridae, burst from obscurity with spectacular outbreaks of severe, haemorrhagic fever. It was first associated with an outbreak of 318 cases and a case-fatality rate of 90% in Zaire and caused 150 deaths among 250 cases in Sudan. Smaller outbreaks continue to appear periodically, particularly in East, Central and southern Africa. In 1989, a haemorrhagic disease was recognized among cynomolgus macaques imported into the United States from the Philippines. Strains of Ebola virus were isolated from these monkeys. Serologic studies in the Philippines and elsewhere in Southeast Asia indicated that Ebola virus is a prevalent cause of infection among macaques (Manson 1989).

These threadlike polymorphic viruses are highly variable in length apparently owing to concatemerization. However, the average length of an infectious virion appears to be 920 nm. The virions are 80 nm in diameter with a helical nucleocapsid, a membrane made of 10 nm projections, and host cell membrane. They contain a unique single-stranded molecule of noninfectious (negative sense ) RNA. The virus is composed of 7 polypeptides, a nucleoprotein, a glycoprotein, a polymerase and 4 other undesignated proteins. Proteins are produced from polyadenylated monocistronic mRNA species transcribed from virus RNA.

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The replication in and destruction of the host cell is rapid and produces a large number of viruses budding from the cell membrane. Epidemics have resulted from person to person transmission, nosocomial spread or laboratory infections. The mode of primary infection and the natural ecology of these viruses are unknown. Association with bats has been implicated directly in at least 2 episodes when individuals entered the same bat-filled cave in Eastern Kenya. Ebola infections in Sudan in 1976 and 1979 occurred in workers of a cotton factory containing thousands of bats in the roof.

However, in all instances, study of antibody in bats failed to detect evidence of infection, and no virus was isolated form bat tissue. The index case in 1976 was never identified, but this large outbreak resulted in 280 deaths of 318 infections. The outbreak was primarily the result of person to person spread and transmission by contaminated needles in outpatient and inpatient departments of a hospital and subsequent person to person spread in surrounding villages. In serosurveys in Zaire, antibody prevalence to Ebola virus has been 3 to 7%. The incubation period for needle- transmitted Ebola virus is 5 to 7 days and that for person to person transmitted disease is 6 to 12 days.

The virus spreads through the blood and is replicated in many organs. The histopathologic change is focal necrosis in these organs, including the liver, lymphatic organs, kidneys, ovaries and testes. The central lesions appear to be those affecting the vascular endothelium and the platelets. The resulting manifestations are bleeding, especially in the mucosa, abdomen, pericardium and vagina. Capillary leakage appears to lead to loss of intravascular volume, bleeding, shock and the acute respiratory disorder seen in fatal cases.

Patients die of intractable shock. Those with severe illness often have sustained high fevers and are delirious, combative and difficult to control. EBOLA SEROLOGY The serologic method used in the discovery of Ebola was the direct immunofluorescent assay. The test is performed on a monolayer of infected and uninfected cells fixed on a microscopic slide. IgG- or IgM-specific immunoglobulin assays are performed. These tests may then be confirmed by using western blot or radioimmunoprecipitation. Virus isolation is also a highly useful diagnostic method, and is performed on suitably preserved serum, blood or tissue specimens stored at -70oC or freshly collected.

TREATMENT OF EBOLA No specific antiviral therapy presently exists against Ebola virus, nor does interferon have any effect. Past recommendations for isolation of the patient in a plastic isolator have given way to the more moderate recommendation of strict barrier isolation with body fluid precautions. This presents no excess risk to the hospital personnel and allows substantially better patient care, as shown in Table 2. The major factor in nosocomial transmission is the combination of the unawareness of the possibility of the disease by a worker who is also inattentive to the requirements of effective barrier nursing. after diagnosis, the risk of nosocomial transmission is small. PREVENTION AND CONTROL OF EBOLA The basic method of prevention and control is the interruption of person to person spread of the virus.

However, in rural areas, this may be difficult because families are often reluctant to admit members to the hospital because of limited resources and the culturally unacceptable separation of sick or dying patients from the care of their family. Experience with human disease and primate infection suggests that a vaccine inducing a strong cell- mediated response will be necessary for virus clearance and adequate protection. Neutralizing antibodies are not observed in convalescent patients nor do they occur in primates inoculated with killed vaccine. A vaccine expressing the glycoprotein in vaccinia is being prepared for laboratory evaluation. SELECTIVE PRESSURES AND CONSTRAINTS It is of interest to determine, what, if any, limits are placed on virus variation. Despite high mutation rates and opportunities for genetic reassortment, many factors act to minimize emergence of new influenza A epidemics (Morse and Schluederberg 1988). even though avian and human influenza viruses are widespread (in humans an estimated 100 million infections yearly), pandemic influenza viruses emerge infrequently (every 10-40 years).

Powerful constraints appear to exist since pandemic human influenza strains vary in their H gene, whereas the neuraminidase and most other genes are conserved. These constraints on viral evolution are not surprising when one considers the selective pressures imposed by the host at each stage of the virus life cycle. Tissue tropism determinants, include site of entry, viral attachment proteins, host cell receptors, tissue- specific genetic elements (for example promoters), host cell enzymes (like proteinase), host transcription factors, and host resistance factors such as age, nutrition and immunity. Host factors contribute significantly: sequences such as hormonally responsive promoter elements and transcriptional regulatory factors can link viral expression to cell state. The interaction of virus and host is thus complex but highly ordered, and can be altered by changing a variety of conditions.

Unlike bacterial virulence, which is largely mediated by bacterial toxins and virulence factors, viral virulence often depends on host factors, such as cellular enzymes that cleave key viral molecules. Because virulence is multigenic, defects in almost any viral gene may attenuate a virus. For example, some reassortments of avian influenza viruses are less virulent in primates than are either parental strain, indicating that virulence is multigenic (Treanor and Murphy 1990). Viral and host populations can exist in equilibrium until changes in environmental conditions shift the equilibrium and favour rapid evolution (Steinhauer and Holland 1987). It seems reasonable to expect that new viruses will emerge occasionally, but the stochastic and mu …