To determine the genetic distance between strains, Sanchez's team focused their attention on the genes in which the viruses differ the most. Since all Ebola strains are known to have jumped species--from their presumed natural hosts to monkeys and humans--the researchers predicted that the greatest variations would occur among the genes which give the virus its ability to recognize different cell species. In the case of Ebola, the most relevant gene turned out to be the glycoprotein gene, which produces proteins that sit on the virus's surface and are thought to shuttle the virus inside the host cell. The CDC group has since looked at other parts of the Ebola genome; so far, the glycoprotein gene does in fact seem the most variable, Nichol reports.
Choosing to analyze the glycoprotein gene allowed an added insight: it revealed that filoviruses, in addition to killing their victims by destroying the cells they infect, might work by suppressing the immune system. This may be one of the reasons they are so deadly. Sanchez's team found that a section of the filovirus glycoprotein gene is very similar to the corresponding sections of the glycoprotein genes in other viruses whose function is to subdue the immune system. Indeed, Ebola victims usually die without evidence of an effective immune response.
A related line of research concerns the search for an animal "reservoir," the hiding place where the Ebola resides during the long stretches between human outbreaks. Scientists don't yet know in which creature or creatures Ebola lies dormant, but groups from the CDC, the World Health Organization and the U.S. Army are all currently screening hundreds of African animal species in search of the reservoir. Whatever it is, the high degree of similarity between the 1976 and 1995 Ebola strains in Zaire (less than 1.6 percent change in the studied RNA segments) suggests to the CDC team that the reservoir is the same in both locations and that the creature is either widespread in Zaire, or else is a migratory species.
On the other hand, the four Ebola strains, along with the Marburg virus, show genetic divergences as great as 45 percent. Such marked differences hint that the various filoviruses are carried by more than one species. Each strain may have slowly co-evolved to live comfortably with their own as yet unknown hosts.
Compared to other less spectacular but more widely distributed illnesses such as tuberculosis and hepatitis, Ebola actually poses a rather limited threat: precisely because it kills its victims so quickly, it cannot easily spread. Yet all pathogens mutate, sometimes leading to the appearance of more pernicious versions (as demonstrated by the emergence of drug-resistant strains of TB). Virologists are continuing their studies of the genetics of filoviruses, hoping to find a treatment or a vaccine. But even if they ever do, the threat that Ebola will reappear, like so many other pathogens, will always remain.