Research Professor of Pathology and Genomic Medicine, Academic Institute
Full Research Member, Research Institute
After earning his PhD in Molecular Biology in 1995 from Northwestern University, Dr. Beres completed post-doctoral fellowships at Baylor College of Medicine and the National Institute of Allergy and Infectious Diseases. Dr. Beres joined the Houston Methodist Research Institute HMRI at its inception in 2006, where he is currently a Full Research Member, Research Institute, Professor, Academic Institute, and Director of Microbial Informatics for the Center for Molecular and Translational Human Infectious Disease Research. Dr. Beres’s research focuses on employing bacterial whole-genome sequencing to understand human infectious diseases caused by microbial pathogens, including Streptococcus pyogenes, Staphylococcus aureus, and Klebsiella pneumoniae.
The primary focus of Dr. Beres’s research is identifying the genetic/genomic basis for intrinsic differences and adaptive changes in the pathogenic behavior of human bacterial infections. Over the last 17 years, Dr. Beres has used bacterial pathogen whole-genome sequencing and related genome-scale strategies on populations of hundreds to thousands of human clinical isolates to obtain initial genomic assessments. Dr. Beres has then used DNA sequencing to further analyze strain-to-strain variation in gene content and RNA/cDNA sequencing for genome-wide gene transcriptome assessment. Dr. Beres is one of few specialists who has focused particularly on the human bacterial pathogen S. pyogenes, colloquially referred to as the “flesh-eating” bacteria. Dr. Beres’s research has contributed 40 of 166 (24%) of the complete genome sequences for S. pyogenes that are currently in the National Center Biotechnology Information GenBank database.
One prominent theme of Dr. Beres’s research has been the use of population pathogenomics to determine the molecular genetic underpinnings responsible for the epidemic shifts of different S. pyogenes genotypes that are responsible for severe invasive infections with high human morbidity and mortality. One important discovery of his research is that recurrent epidemic waves of type emm3 S. pyogenes stemmed from the emergence of newly evolved strains with enhanced fitness, and not from recycling of the same clone responsible for the preceding wave. Similarly, his analysis of 3,615 samples of type emm1 S. pyogenes obtained from global sources found that only four molecular genetic events were responsible for the pandemic of severe invasive infections worldwide. He also discovered that an emm89 S. pyogenes epidemic clone evolved through a complex series of multiple horizontal-transfer genetic recombination events, one of which was virtually identical to the recombination event responsible for triggering the pandemic of invasive infections caused by the emm1 strain. These three studies are some of the largest population pathogenomic infectious disease investigations that have been conducted.