Discipline: Biological Sciences
Subcategory: Microbiology/Immunology/Virology
Session: 3
Selena N. Williams - North Carolina Agricultural and Technical State University
Co-Author(s): Scott H. Harrison, North Carolina Agricultural and Technical State University, Greensboro, NC
Influenza is responsible for 290,000 to 650,000 deaths worldwide per year. Our research seeks to expand on the evolutionary relationships between lineages of influenza, and pursue a phylodynamic study of epidemic and pandemic capabilities. We hypothesize that the more virulent strains will have a phylogenetic tree topology with greater asymmetry, where this asymmetry is expected based on how there may be strong selection for lineages that are more aggressive in the infection and attack of hosts. The influenza virus is divided into four types – A, B, C, and D – across which we base our analytical comparison. Type A and B are classified as epidemic strains. Type A can transmit between different human, livestock and other hosts, while Type B is mostly found in human populations. Most research has focused on the subtypes of influenza A virus (H1N1 and H3N2), and more recently diverged lineages of influenza type B (B/Yamagata and B/Victoria). Type C rarely infects human populations and results in mild respiratory illness, while Type D reportedly only infects cattle. Although scientists state that types C and D are not pandemic, little research has been conducted on the differences between these influenza types. Our methodology is to quantify phylogenetic tree topologies within and between these different types of influenza, and model how asymmetry relates to virulence and outbreaks, by phylogenetic reconstructions on hemagglutinin and hemagglutinin-esterase genes. We then validate this inferential treatment with an examination of the historical record and associated geographic locations of the different lineages and phylogenetic groupings through the Influenza Research Database (http://www.fludb.org). We generally found this approach to be effective, for how virulence and asymmetry would correlate, based on both influenza variety, and reports in the historical record. This work shows how modeling genetic change over time can aid in the objective identification of virulence, and we now seek to further develop this overall potential of phylodynamic modeling through examinations of other influenza genes experiencing selection.
Funder Acknowledgement(s): This work was supported by the National Science Foundation (NSF) under Grants HRD-1623358 and HRD-1719498. Any opinions, findings, and conclusions or recommendations expressed in this work are those of the authors and do not necessarily reflect the views of the funding agency.
Faculty Advisor: Scott H. Harrison, scotth@ncat.edu
Role: I researched different varieties of influenza, major epidemics, genetics of influenza, and conducted a literature review of prior phylogenetic modeling of influenza. I utilized past work of mine in tree topology measurement methodologies for this study. I furthermore was the primary person of my laboratory to first learn about and then use most all of the extensive features of the Influenza Research Database (http://www.fludb.org). I put together all elements of this report.