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Evolution of Ebola and Marburg viruses

References:

Carroll, S. A., J. S. Towner, T. K. Sealy, L. K. Mcmullan, M. L. Khristova, F. J. Burt, R. Swanepoel, P. E. Rollin, and S. T. Nichol. "Molecular Evolution of Viruses of the Family Filoviridae Based on 97 Whole-Genome Sequences." Journal of Virology 87.5 (2013): 2608-616. Web.

Hensley, Lia E., Sabue Mulangu, Clement Asiedu, Joshua Johnson, Anna N. Honko, Daphne Stanley, Giula Fabozzi, Stuart T. Nichol, Thomas G. Ksiazek, Pierre E. Rollin, Victoria Wahl-Jensen, Michael Bailey, Peter B. Jahrling, Mario Roederer, Richard A. Koup, and Nancy J. Sullivan. "Demonstration of Cross-protective Vaccine Immunity against an Emerging Pathogenic Ebolavirus Species." PLoS Pathogens 6.5 (2010): n. pag. Web.

Li, Y. H., and S. P. Chen. "Evolutionary History of Ebola Virus." Epidemiology & Infection 142.6 (2014): 1138-145. Web.

Mackenzie, Debora. "Ebola Evolves Deadly New Tricks." New Scientist 196.2625 (2007): 12. Web.

Suzuki, Y., and T. Gojobori. "The Origin and Evolution of Ebola and Marburg Viruses." Molecular Biology and Evolution 14.8 (1997): 800-06. Web.

Proposed Changes

https://en.wikipedia.org/wiki/Talk:Ebolavirus

Actual Changes Made

https://en.wikipedia.org/wiki/Ebolavirus
 * Added 3 sentences discussing the genetic differences of Ebolavirus and Marburgvirus in the "evolution" section

Final Paper Starts Here

The Evolution of Marburg and Ebola Virus

Ebola is currently a “hot topic” in the media. The outbreak in West Africa has claimed 4881 lives as of October 22, 2014 and threatens many more. There are 5 identified strands of Ebola in the Ebolavirus genus. There is Ebola virus (EBOV) or Zaire ebolavirus (this is responsible for the current outbreak in West Africa), Sudan ebolavirus (SUDV), Reston ebolavirus (RESTV), Tai Forest ebolavirus (TAFV) and Bundibugyo ebolavirus (BDBV) (Wikipedia: Ebolavirus). In addition to the 5 strands of Ebola, there is their closely related cousins, Marburg virus and Ravn virus. All 7 of these viruses began to diverge from each other several thousand years ago, but the virus family can be traced to being a couple million years old. Even though all these viruses are related, both genetically and with the symptoms shown, there are some significant differences between them all. The virus was first discovered during the 1970’s, during the first few Ebola outbreaks. After the first few outbreaks, there was an outbreak hiatus, with the next outbreaks beginning during the mid 1990’s. After this hiatus, the virus had changed its genetic structure and presented differently when compared to the 1970’s version (Suzuki, 600). A study that looked at the two different strands of Ebola, one from the original 1976 outbreak and the post-hiatus strand from 1995 outbreak, found that there was a 2% difference in the genetic structure of the virus (Sanchez, 3602) Although viruses do not fit the criteria, such as having a cellular structure or are able to self-reproduce, to be considered alive, they still experience evolutionary forces such as selection, migration and bottlenecks.

Understanding how the virus is carried, replicated and transmitted will show where evolutionary forces can affect something that isn’t living. Ebola resides in primates, primarily bats and monkeys, or in the case of Ebola Reston, pigs. It is believed that Ebola Reston has recently evolved to effect pigs. Originally, the virus was found to originally effect macaques (the outbreak was in Reston, Virginia, in a primate handling facility), but there have been recent outbreaks in domesticated pigs in the Philippines (Miranda, 757). Humans have been affected with Ebola Reston, but the virus has no ill effects similar to the other strands of Ebola. Ebolavirus is contained in bodily fluids, and transmitted through contact with the infected bodily fluids. In laboratory experiments, the virus was shown to have the ability be transmitted through the air via airborne bodily fluids, but it was shown not to be able to affect humans. In primates, the hallmark trait of having Ebola is a significant release of bodily fluids (hemorrhagic fever), with the goal of these fluids reaching another potential host (Wikipedia: Ebolavirus). Once the virus has found a new suitable host, it will then replicate and the process will continue. Ebola experiences the majority of evolutionary forces through its hosts. Ebola has evolved to affect only certain primates. Taking humans for example, all strains of Ebola effect humans except for Ebola Reston. Ebola Reston also effects domesticated pigs, where it is unknown whether the other strains of Ebola will have an effect (Miranda, 757). Ebola seems to have evolved to ability to effect the primates that exist in a specific region. Looking specifically at Ebola Reston, there is a 4% difference between the nucleotide chains of the monkey strand and the pig strand (Boehmann, 417). This suggests that Ebola is able to evolve in a way to “jump” from one primate species to another, though the virus may not be able to spread via hemorrhagic fever initially (Ebola Reston is able to exist in humans, but it does not spread vie hemorrhagic fever). This trait that Ebola has is extremely important to the perpetuation of the virus. For the virus to exist, it needs a host. If the virus has the ability to jump from host to host, and isn't limited to one single species, the fitness of the virus increases dramatically. This change in fitness helps explain one question that scientists have about the Ebola outbreaks; “Why was there a 20 year gap in the outbreaks” and “Why, even though this virus family is 10s of millions years old, has the virus only recently been detected”. Both of these questions can be answered by bottlenecks. It is believed that there are an infinite amount of variants for Ebola; Ebola has a unique ability to recombine with other similar strands creating a 3rd new strand (Mackenzie, web). Often these new strands will die out or go dormant. A few strands have affected the lowlands Gorilla, killing a portion of the population. The lowlands gorilla is an endangered species, partially due to hunting and habitat loss, which has caused some of those strains of Ebola to die out (Li, 1138). Though some strains die out, the most fit or in the case of a virus, the most contagious will persist and continue spreading. It is believed that the original strand from the outbreak in 1976 had died out, but the hemorrhagic fever component persisted, and 20 years later a better and stronger version of the virus caused another outbreak (Li, 1138).

Continuing with how evolution forces effect Ebola through the host, one significant force is evident. Migration of the host has a significant effect on Ebola. Since Ebola relies of its host, anything that happens to the host will happen to the virus, if the host dies, then the virus dies, and if the host moves, then the virus moves (Miranda, 757). Ebola Reston is a good example of this migration. Ebola Reston has been linked to monkeys in the Philippines, where Ebola Sudan, the most similar strain of Ebola to Ebola Reston is located primarily in Sudan located in the heart of Africa. Very little is actually known as to how Ebola Reston has ended up in the Philippines, so there is a lot of speculation as to how, but regardless to how it got there, the virus was definitely carried by some host from Africa to the Philippines. This migration of the host caused a new species to form.

The most influential evolutionary force is mutation. The rate of mutation for Ebola virus and Marburg virus has been studied heavily and has given scientists a relatively good idea of where and how Ebola and Marburg have developed. The rate of Ebola has been determined to be 3.6 x10-5 mutations per site per year (Suzuki, 800). That is approximately 100x less than Human influenza virus and about the same rate as the Hepatitis B virus. Marburg virus has approximately the same mutation rate. When the nucleotide structures of Marburg virus and Ebola virus are compared, along with looking at fossil records, the two seem to have diverged from each other at least several thousand years ago; records show that this family of viruses are at least 10s of millions years old (paleoviruses have been found in mammals dating back millions of years) (Suzuki, 800). On the nucleotide level, there is approximately a 55% difference between the two, with a 67% difference in the amino acid level. Looking specifically at Ebola, there is about a 37-41% variance among all the strands at the nucleotide level; at the amino acid level there is about a 34-43% difference. Most shocking is the fact that in about 20 years, Ebola Zaire had about a 2% change in its nucleotide level (Sanchez, 3602). Along with that 2 difference, there was an emergence of 2 slightly deferent strains, 2 subspecies per say, which emerged. These 2 strains have been shown in the lab to be able to recombine with each other to create new strains (Mackenzie, web). This has also been shown to happen in other strains as well. This recombination ability is unique to Ebola, with no other filovirus being able to do this, thus giving Ebola the ability to evolve new traits extremely quickly.

Changes at the nucleotide level are what drive the evolution of all living things and even Ebola. Although not a living being, Ebola still faces evolutionary pressures that affect living creatures. Evolutionary forces such as selection, bottlenecks and migration cause Ebola to change and diversify. Ebola has to evolve, so that it can increase its fitness, and so that its genetic material get passed on. This need to evolve has created the many different strains of Ebola today, including the strain that has broken out in West Africa. Understanding where and how evolution effect Ebola, can help control Ebola preventing future outbreaks from occurring and stronger strains from appearing.

References

Boehmann, Yannik, Sven Enterlein, Anke Randolf, and Elke Muhlberger. "A Reconstituted Replication and Transcription System for Ebola Virus Reston and Comparison with Ebola Virus Zaire." Virology 332.1 (2005): 406-17. Web.

"Ebolavirus." Wikipedia.com. N.p., 28 Oct. 2014. Web.

Hensley, Lia E., Sabue Mulangu, Clement Asiedu, Joshua Johnson, Anna N. Honko, Daphne Stanley, Giula Fabozzi, Stuart T. Nichol, Thomas G. Ksiazek, Pierre E. Rollin, Victoria Wahl-Jensen, Michael Bailey, Peter B. Jahrling, Mario Roederer, Richard A. Koup, and Nancy J. Sullivan. "Demonstration of Cross-protective Vaccine Immunity against an Emerging Pathogenic Ebolavirus Species." PLoS Pathogens 6.5 (2010): n. pag. Web.

Li, Y. H., and S. P. Chen. "Evolutionary History of Ebola Virus." Epidemiology & Infection 142.6 (2014): 1138-145. Web.

Mackenzie, Debora. "Ebola Evolves Deadly New Tricks." New Scientist 196.2625 (2007): 12. Web.

Miranda, Mary E., and Noel L. Miranda. "Reston Ebolavirus in Humans and Animals in the Philippines: A Review." Journal of Infectious Diseases (2011): 757-60. Web.

Sanchez, Anthony, Sam G. Trappier, Brian W. J. Mahy, Clarence J. Peters, and Stuart T. Nichol. "The Virion Glycoprotiens of Ebola Viruses Are Encoded in Two Reading Frames and Are Expressed through Transcriptional Editing." JSTOR. N.p., n.d. Web. 28 Oct. 2014.

Suzuki, Y., and T. Gojobori. "The Origin and Evolution of Ebola and Marburg Viruses." Molecular Biology and Evolution 14.8 (1997): 800-06. Web.