Over the past few weeks, I’ve made no secret about my growing love for medical anthropology. I’ve been dying to try and make a connection between primatology and medical anthropology, but for weeks, I haven’t been able to think of anything–that is, until now.
Peter Walsh, a primatologist affiliated with the Max Planck Institute for Evolutionary Anthropology, has set up an initiative to establish a working vaccine for ebola to protect populations of African great apes from the viral disease. Ebola is responsible for killing one-third of the gorilla population and a sizable amount of chimpanzees in the last twenty years (Walsh et al. 2007). With that in mind, creating a working vaccine seems like a worthwhile solution: prevent these (critically, in some cases) endangered primates from losing group members by creating a vaccine that is responsible for killing up to a third of the population.
Or does it? I have some reservations, but I’ll get into that a little while.
Ebola: Nightmares are made of this

An electron micrograph of the ebola virus. This is the thing nightmares are made of. (Photo from: WikiMedia Commons)
As stated previously, ebola is a virus; a zoonotic virus that not only infects our primate kin, but ourselves as well (which I’ll get into a little later.) Ebola was originally recognized in 1976 in the western equatorial province of Sudan and what is now the Democratic Republic of Congo (previously, Zaire.) Overall, there are five specific subtypes currently discovered that have been confirmed in Sudan, Gabon, Uganda, Republic of Congo, the Ivory Coast, and the Democratic Republic of Congo.
Currently, fruit bats (Epomops franqueti, Hypsignathus monstrosus, and Myonycteris torquata) are thought to be the natural host species, or reservoir of the Zaire virus (Pourrut et al. 2007). The Zaire virus strain is considered the most virulent and devastating to chimpanzee, gorilla, and human populations.
The ebola virus is believed to be transmitted from bat-to-bat by both vertical means (mother-to-offspring) and horizontal (infected bat biting non-infected bat or via mating); still, the link between transmission from bats to great apes and humans has yet to be found. However, there is a potential ecological hypothesis which posits during the end of the rainy season and beginning of dry season in Africa (November to February), fruit abundance is at its highest peak which is a primary food source for both great apes and fruit bats. It is possible that when bats consume and drop partially eaten fruits or pulp, the fluids from the bat would remain and contaminate great apes that consume the fruit (Gonzalez et al. 2007). Ebola can also be spread via aerosols in breathable droplets (Johnson et al. 1995). However, given that fruit bats and great apes do not typically share the same niche in the ecosystem, the contamination of partially eaten fruit is a more likely option.
Apes, Humans, and Vaccines: Naturally Selected for Each Other?

When I think of bushmeat, this is the image that always comes to mind. A gorilla's head used for cooking purposes. (Photo by: Karl Ammann)
While this seems likely for great apes, this does not explain how humans become initially infected with the ebola virus. However, evidence is beginning to suggest that the zoonotic origin of the human infection comes from bushmeat hunting (Rouquet et al. 2005). In a 1996 outbreak in Gabon, an epidemiological survey showed that index case-patients were infected by physical contact with an infected chimpanzee.
And now, the skepticism part: there has been a live attenuated vaccine developed by Integrated BioTherapeutics Inc. that has proven efficacy in establishing a challenge to the virus dose in rhesus macaques. Walsh intends to use this in experiments in chimpanzees with later use in gorillas, as well.
The practice of vaccinating wildlife is sometimes risky; live attenuated could always cause disease and/or revert to virulent pathogen because of selection pressures caused by vaccinations. (Think: MRSA and antibiotics in humans.) In a species such as gorilla, where it may be difficult to track populations down, this may prove to become a costly endeavor.
In terms of selection pressures, ebola viruses mutate at about the same rate (10-5 to 10-4 per site per year) as many other RNA viruses. Although slower than influenza A and retroviruses, it does undergo a rapid evolution comparatively (Suzuki & Gojobori 1999). That said, while not as large of a risk, there is still a potential for mutation within the virus to occur.
Ebola and Bushmeat: Under Pressure
So what does this mean for humans? Well, for one: the vaccine is only produced for great apes so far. Yet, there are examples of other forms of bushmeat (i.e. duikers) that have been historically contaminated with the virus as well (Leroy et al. 2004). This means that while we may have protection in one form of bushmeat, many other forms can expose humans to ebola pathogens as well.
Second, it is true that ebola does kill a third of the gorilla population and also has a significant toll on chimpanzee populations—what about the other two-thirds? As Walsh et al. (2007) suggest, the other significant players in the role of gorilla deaths tend to be bushmeat hunting and habitat loss. Given the fact that bushmeat plays a role in both transmission of the virus and population declines for gorilla, perhaps it would be more effective to examine the bushmeat trade.
I’m not suggesting that we give up on this idea quite yet; it is absolutely worthwhile to pursue a vaccine which will protect chimpanzees and gorillas. However, I am saying that before we get too excited about eliminating one ultimate cause that we perhaps examine the “big picture” a little more—before there’s ultimately a bigger problem at hand.
References
Gonzalez JP, Pourrut X, & Leroy E (2007). Ebolavirus and other filoviruses. Current topics in microbiology and immunology, 315, 363-87 PMID: 17848072
Johnson, E., Jaax, N., White, J., & Jahrling, P. (1995). “Lethal experimental infections of rhesus monkeys by aerosolized Ebola virus.” International journal of experimental pathology 76(4): 227–36.
Leroy, E.M, Rouquet, P, Formenty, P., Souquière, S., Kilbourne, A., Froment, J.M., Bermejo, M., Smit, S., Karesh, W., Swanepoel, R., Zaki, S.R., & Rollin, P.E. (2004). Multiple Ebola virus transmission events and rapid decline of central African wildlife. Science (New York, N.Y.), 303 (5656), 387-90 PMID: 14726594
Pourrut X, Délicat A, Rollin PE, Ksiazek TG, Gonzalez JP, & Leroy EM (2007). Spatial and temporal patterns of Zaire ebolavirus antibody prevalence in the possible reservoir bat species. The Journal of Infectious Diseases, 196 Suppl 2 PMID: 17940947
Rouquet, P., Froment, J.M., Bermejo, M., Kilbourn, A., Karesh, W., Reed, P., Kumulungui, B., Yaba, P., Délicat, A., Rollin, P.E., & Leroy, E.M. (2005). Wild animal mortality monitoring and human Ebola outbreaks, Gabon and Republic of Congo, 2001-2003. Emerging Infectious Diseases, 11 (2), 283-90 PMID: 15752448
Suzuki, Y. Gojobori, T. (1999). A method for detecting positive selection at single amino acid sites. Mol. Biol. Evol., 16: 1315-1328.
Walsh, P.D., Tutin, C.E.G., Oates, J.F., Baillie, J.E.M., Maisels, F., Stokes, E.J., Gatti, S., Bergl, R.A., Sunderland‐Groves, J., & Dunn. A. (2007). Gorilla gorilla. In: 2007 IUCN Red List of Threatened Species, IUCN.<www.iucnredlist.org>
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The live attenuated poliovirus vaccines revert to neurovirulence in each recipient and can cause outbreaks of poliomyelitis. Therefore the possibility of reversion to virulence of an ebola live attenuated vaccine is not far from reality. The vaccine needs to be tested for genetic stability in primates before it is released. A better strategy would be to use an ebolavirus protein vectored by, say, vaccinia virus. As is done to immunize wild animals against rabies virus.
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