Abstract

The purpose of this project is to analyze the evolution of the Ebola virus. After the latest outbreak enough Ebola strains have been sequenced to allow a through evolutionary study. Comparing patterns of mutation in regions that have been identified as epitopes to non-epitope protein regions will allow conclusions to be drawn regarding Ebola’s interaction with the human immune system and whether it will remain a deadly acute disease. If the regions have a universal level of mutation, then there is no sign of immune pressure. This means that the virus is not changing in response to interaction with the human immune system. If this is the case, Ebola will remain an acute infection and probably a very deadly one. However, if there are patterns of higher rates of evolution in epitope regions Ebola may become more acclimated to humans and transition to a less fatal or chronic disease. This behavior is seen in influenza where a highly virulent strain often evolves to be less deadly. There is evidence already that Ebola can be an asymptomatic infection in some cases. The reservoir of the Ebola virus is still unknown. Whether the virus is an acute or chronic infection in its reservoir is also unknown. If it is a chronic disease in its reservoir host then it has the ability to become chronic in humans. Thus, I am mapping point mutations in the Ebola virus protein and ascertaining whether or not these mutations are in regions of structural or antigenic importance.

Modified Abstract

The purpose of this project is to analyze the evolution of the Ebola virus. After the latest outbreak, enough Ebola strains have been sequenced to allow a thorough evolutionary study. Comparing patterns of mutation in regions that have been identified as epitopes to non-epitope protein regions will allow conclusions to be drawn regarding Ebola’s interaction with the human immune system. Ebola could also possibly become more acclimated to humans and transition to a less fatal or chronic disease. If it is a chronic disease in its reservoir host, then it has the ability to become chronic in humans. Thus, I am mapping point mutations in the Ebola virus protein and ascertaining whether or not these mutations are in regions of structural or antigenic importance.

Research Category

Biology/Ecology

Author Information

Chanelle D. WaliguraFollow

Primary Author's Major

Biology

Mentor #1 Information

Dr. Olena Piontkivska

Mentor #2 Information

Mary Saha (Halpin)

Presentation Format

Poster

Start Date

21-3-2017 1:00 PM

Research Area

Biology

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Mar 21st, 1:00 PM

Molecular Evolution of Immune Epitopes in Ebola Virus (EBOV, Filoviridae): Insights Into Host-Pathogen Interactions

The purpose of this project is to analyze the evolution of the Ebola virus. After the latest outbreak enough Ebola strains have been sequenced to allow a through evolutionary study. Comparing patterns of mutation in regions that have been identified as epitopes to non-epitope protein regions will allow conclusions to be drawn regarding Ebola’s interaction with the human immune system and whether it will remain a deadly acute disease. If the regions have a universal level of mutation, then there is no sign of immune pressure. This means that the virus is not changing in response to interaction with the human immune system. If this is the case, Ebola will remain an acute infection and probably a very deadly one. However, if there are patterns of higher rates of evolution in epitope regions Ebola may become more acclimated to humans and transition to a less fatal or chronic disease. This behavior is seen in influenza where a highly virulent strain often evolves to be less deadly. There is evidence already that Ebola can be an asymptomatic infection in some cases. The reservoir of the Ebola virus is still unknown. Whether the virus is an acute or chronic infection in its reservoir is also unknown. If it is a chronic disease in its reservoir host then it has the ability to become chronic in humans. Thus, I am mapping point mutations in the Ebola virus protein and ascertaining whether or not these mutations are in regions of structural or antigenic importance.