EBOLA
Filoviruses are, without a doubt, one of the deadliest viruses in the world. Epidemics in Northern Zaire in 1976 had a mortality rate of 88% -- only HIV and rabies have recorded higher rates. It kills within a week and causes severe bleeding as well as clotting. All body tissues become highly infectious (Preston, 1992). Nevertheless, little is known about the virus' means of primary infection and the natural ecology of Ebola and its sibling Marburg, despite careful research in the areas where the virus is thought to have originated (Jacobson, 1994).
The first filovirus outbreak occured in 1967 in Marburg, Germany, and Yugoslavia, when a shipment of African green monkeys infected 25 people working with the monkeys with a severe hemorrhagic fever. Six additional medical staff and family members became infected after the initial outbreak, and a total of seven died from the disease.
Marburg struck again in 1975, killing one traveller in Zimbabwe and infecting two others. A new epidemic soon followed one year later in Northern Zaire, killing 280 out of 318 people. However, this was a new strain of filovirus, morphologically similar to Marburg but immunologically distinct. Scientists named it 'Ebola', after a small river in Zaire where the first case was thought to have come from. Ebola was spread through close contact at hospitals, use of contaminated needles and syringes, and close contact during the burial process (Peters, Sanchez, Feldmann, Rollin, Nichol, Ksiazek, 1994; World Health Organization, 1978).
At the same time, Ebola was making itself known in Southern Sudan. Although the official World Health Organization (WHO) report implies an as yet undiscovered link between the two outbreaks, Joe McCormick of the Centers for Disease Control in Atlanta (CDC) insists that there could have been no contact between people of the two areas. He traveled to N'zara, Sudan from Yambuku, Zaire via Land Rover and found no Ebola cases in the villages between the cities. "There's no way the Yambuku epidemic could get to N'zara or vice-versa unless some infected person traveled those roads. And...my Land Rover was the first vehicle on those so-called roads in months...maybe years." (Garrett, 1994). Later research proved McCormick's hypothesis when the Zaire and Sudan strains were found to be genetically distinct (Cox, et al., 1983).
Ebola Sudan had a lower mortality rate than Ebola Zaire (53%) but was spread in much the same way; by close contact with infected people and use of contaminated needles by hospital staff (Peters, Sanchez, Feldmann, Rollin, Nichol, Ksiazek, 1994). The virus was not considered to be transmitted by airborne particles or droplets (WHO, 1978).
Single cases of Ebola and Marburg continued to occur sporadically between 1977 and 1987, mostly in Central Africa. But in 1989, a shipment of monkeys to Reston, Virginia, a suburb of Washington D.C., fell sick with a disease symptomatically similar to simian hemorrhagic fever (SHF). Tests were done at the U.S. Army Medical Research Institute of Infectious Diseases (USAMRIID), and three of the ten animals tested were positive for SHF. However, that was not the only virus circulating around their systems. Five of the ten monkeys tested positive for Ebola. Before this incident, no monkey had ever been found to be naturally infected with the Ebola virus (Dalgard et al. 1989). More importantly, monkeys in cages kept across the room from infected monkeys suddenly became sick. They had never had contact with the sick monkeys. "It got there somehow," Col. Nancy Jaax said. "When the caretakers wash the cages down with water hoses, that can create an aerosol of droplets. It probably traveled through the air in aerosolized secretions. That was when I knew that Ebola can travel through the air." (Preston, 1994).
In humans, monkeys, and guinea pigs, the mechanism of recovery is unknown. Neutralizing antibodies have not been observed in survivors of Ebola Ð ruling out the possibility of an antiserum Ð and furthermore, the viruses are resistant to the in vitro antiviral actions of inteferons or the antiviral drug Ribavirin. (Peters, Sanchez, Rollin, Ksiazek, Murphy, 1994; Jacobson, 1994). Thus, cell mediated immunity is the major candidate to mediate recovery, although proof has not been presented. In fatal filovirus infections, the host dies with generally no evidence of an immune response. The reason for the failure is unknown (Peters, Sanchez, Rollin, Ksiazek, Murphy, 1994).
Marburg and Ebola are quite infective at room temperature but are destroyed in 30 minutes when heated at 60 degrees Celsius. Infectivity is also destroyed by UV and gamma irradiation, lipid solvents, detergents, and common disinfectants (Peters, Sanchez, Feldmann, Rollin, Nichol, Ksiazkek, 1994; Peters, Jahrling, Ksiazek, Johnson, Lupton, 1992).
Because we have so little information on the history of filoviruses, and because research to find a natural reservoir of the virus has come up short, we are unable to predict or control the development of epidemics. As the opportunity for faster travel increases to allow more movement within an incubation period, so does the probability of human encounters with filoviruses.
Could mutants of filoviruses with increased potential for causing "serious trouble" arise? It is more than likely, given that all RNA viruses have the potential for rapid evolution because of the high error rate of RNA polymerases that they use to replicate their genomes. Therefore, disregarding the fact that there are already a high number of genetic variations among filoviruses, the number of different strains of filovirus can only increase. The genomes are shaped by their host system, and the host selects variants in transmissibility, virulence, and other properties. Filoviruses already enjoy high primate pathogenicity, host-to-host transmissibility, and in some cases, aerosol infectivity (Peters, Sanchez, Feldmann, Rollin, Nichol, Ksiazek, 1994). As the human population and speed of travel increase, we can only wait for the virus to come to us. Only by increasing our knowledge of the genetics, pathogenesis, and natural history of filoviruses can we decrease the danger.
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