Thomas A. Hooven, MD
- Assistant Professor, Department of Pediatrics
- Scholar, Richard King Mellon Foundation Institute for Pediatric Research
Education & Training
- MD, University of Michigan Medical School, 2007
- BA in Psychology, Yale University, 2001
Our research seeks to address the problem of serious bacterial infections that affect newborns. These infections can be life threatening and many are associated with long-term complications that create challenges for growing children and their families for years to come. Our group seeks to understand the molecular interactions between babies and bacteria that give rise to these infections. Why do some bacteria cause infections in newborns but rarely in older children and adults? How do babies protect themselves from the many billions of new bacteria that they encounter in the first few weeks of life? Can a better understanding of neonatal immunity help drive new treatments to reduce the burden of serious bacterial infections during this uniquely vulnerable period of life? These are the kinds of questions we seek to answer through molecular and genetic investigations of newborns, bacteria, and their interactions. One of our main areas of focus is group B Streptococcus, a Gram-positive pathobiont that can cause chorioamnionitis (infection of the placenta and the fetus), neonatal sepsis, pneumonia, and meningitis. We use a combination of bioinformatics, in vitro screens, and animal models to better understand group B Streptococcal virulence factors and the environmental signals that regulate them. Another active area of research is using advanced modeling and machine learning approaches to identify causes of necrotizing enterocolitis, a serious neonatal intestinal disease caused in part by abnormal bacterial colonization of the preterm neonatal intestine.
Hooven TA, Lin YC and Salleb-Aouissi A. 2020. Multiple instance learning for predicting necrotizing enterocolitis in premature infants using microbiome data. Proceedings of the ACM Conference on Health, Inference and Learning (ACM CHIL '20). April 2020.
Hooven TA, Bonakdar M, Chamby AB and Ratner AJ. 2019. A Counterselectable Sucrose Sensitivity Marker Permits Efficient and Flexible Mutagenesis in Streptococcus agalactiae. Appl Environ Microbiol. 85: e03009-18.
Hooven TA, Catomeris AJ, Bonakdar M, Tallon LJ, Santana-Cruz I, Ott S, Daugherty SC, Tettelin H and Ratner AJ. 2018. the Streptococcus agalactiae Stringent Response Enhances Virulence and Persistence in Human Blood. Infect Immun. 86: e00612-17.
Hooven TA, Catomeris AJ, Akabas LH, Randis TM, Maskell DJ, Peters SE, Ott S, Santana-Cruz I, Tallon LJ, Tettelin H and Ratner AJ. 2016. The essential genome of Streptococcus agalactiae. BMC Genomics. 17: 406.
Hooven TA, Randis TM, Daugherty SC, Narechania A, Planet PJ, Tettelin H and Ratner AJ. 2014. Complete Genome Sequence of Streptococcus agalactiae CNCTC 10/84, a Hypervirulent Sequence Type 26 Strain. Genome Announc. 2: e01338-14.