Clinical Microbiology: Open Access

Effects of recent human evolution on the genetic basis of infectious disease susceptibility

Joint Event on 8^th Annual Congress on CLINICAL MICROBIOLOGY & INFECTIOUS DISEASES & 13^th World Congress on VIROLOGY, INFECTIONS AND OUTBREAKS

December 05-06, 2018 | Vancouver, Canada

Erik Corona

Cigna, USA

Keynote: Clin Microbiol

Abstract:

Infectious disease has shaped the natural genetic diversity of humans throughout the world. The extreme death rate caused by pathogens led to substantial selective pressure throughout human evolution and may be responsible for the many widespread unidentified selection signals in the human genome. We created a new approach to combine insights from positive selection methods and knowledge regarding infectious diseases protein-protein interactions to shed light on multiple currently unexplained positive selection events. We created a human-pathogen interaction database and used the integrated haplotype score (iHS) to detect recent positive selection in genes that interact with proteins from 26 different pathogens. We used the Human Genome Diversity Panel to identify specific populations harboring pathogen-interacting genes that have undergone positive selection. We found that human genes that interact with 9 pathogen species show evidence of recent positive selection. These pathogens are Yersinia pestis, human immunodeficiency virus (HIV)-1, Zaire ebolavirus, Francisella tularensis, dengue virus, human respiratory syncytial virus, measles virus, Rubella virus and Bacillus anthracis. For HIV-1, GWASs demonstrate that some naturally selected variants in the host-pathogen protein interaction networks continue to have functional consequences for susceptibility to these pathogens. We show that selected human genes were enriched for HIV susceptibility variants (identified through GWAS), providing further support for the hypothesis that ancient humans were exposed to lentivirus pandemics. These results reveal some of the genetic footprints created by pathogens in the human genome that may have left lasting marks on susceptibility to infectious disease.

Biography :

Erik Corona completed his PhD from Stanford University School of Medicine and Postdoctoral studies at Harvard Medical School. He is a Biomedical Informatics Researcher at Cigna where he currently analyzes claims data to understand and improve the quality of care for individuals with various diseases. He co-founded and served as Director of Data Science at Serendipity, a company that developed tools to facilitate the application of machine learning to a variety of diverse data sets. He currently runs a website geneworld.stanford.edu where people can identify populations that have a higher/lower genetic risk for a multitude of complex and infectious diseases.

E-mail: erikcorona@gmail.com