Megan T. Baldridge, M.D., Ph.D.

Associate Professor
Internal Medicine
Infectious Diseases
Molecular Microbiology

Molecular Microbiology and Microbial Pathogenesis Program
Molecular Genetics and Genomics Program
Immunology Program
Computational and Systems Biology Program

  • 314-273-1212

  • 314-273-1220

  • 832-236-4899

  • Room 4204, McKinley Research Building, 4515 McKinley McKinley Ave, St. Louis, MO 63110



  • microbiota, infection, pathogen, microbiome, virus, interferon, immunity

  • Defining the mechanisms behind and effects of the interactions between commensal bacteria, pathogens and innate immunity

Research Abstract:

The Baldridge lab is broadly interested in the complicated interplay between three important factors: commensal microbes, the host immune system, and viral and bacterial pathogens. Previous work has involved characterization of the intestinal commensal microbiota and interrogation of its role in regulation of both enteric viral infection and the host immune system. The coordination of next-generation sequencing efforts with in vivo infections and treatments in mouse models makes the exploration of transkingdom interactions possible. There are several main areas the Baldridge lab is currently pursuing:

1. Determine the cellular source of the inflammatory cytokine interferon-lambda (IFN-λ) in the intestine induced by commensal bacteria and by pathogens, and the signaling pathways and transcription factors that regulate its expression.
2. Define specific commensal bacteria necessary and sufficient to enhance and regulate viral infection in the intestine.
3. Explore viral adaptation strategies to take advantage of commensal microbes and to infect at alternate host sites.
4. Understand how interactions between bacteria and bacteriophage may contribute to microbiota development and disease.

Selected Publications:

Ingle H, Hassan E, Gawron J, Mihi B, Li Y, Kennedy EA, Kalugotla G, Makimaa H, Lee S, Desai P, McDonald KG, Diamond MS, Newberry RD, Good M, Baldridge MT. Murine astrovirus tropism for goblet cells and enterocytes facilitates an IFN-λ response in vivo and in enteroid cultures. Mucosal Immunology 2021. 10.1038/s41385-021-00387-6.

Walker FC, Hassan E, Peterson ST, Rodgers R, Schriefer LA, Thompson CE, Li Y, Kalugotla G, Blum-Johnston C, Lawrence D, McCune BT, Graziano VR, Lushniak L, Lee S, Roth AN, Karst SM, Nice TJ, Miner JJ, Wilen CB#, Baldridge MT#. Norovirus evolution in immunodeficient mice reveals potentiated pathogenicity via a single nucleotide change in the viral capsid. PLOS Pathogens 2021: 17(3):e1009402. #co-corresponding

Graziano VR, Walker FC, Kennedy EA, Wei J, Ettayebi K, Strine MS, Filler RB, Hassan E, Hsieh LL, Kim AS, Kolawole AO, Wobus CE, Lindesmith LC, Baric RS, Estes MK, Orchard RC, Baldridge MT#, Wilen CB#. CD300lf is the primary physiologic receptor of murine norovirus but not human norovirus. PLOS Pathogens 2020: 16(4):e1008242. #equal contribution

Grau KR, Zhu S, Peterson ST, Winesett E, Philip D, Philips M, Hernandez A, Turula H, Frasse P, Graziano VR, Wilen CB, Wobus CE, Baldridge MT#, Karst SM#. The intestinal regionalization of acute norovirus infection is regulated by the microbiota via bile acid-mediated priming of type III interferon. Nature Microbiology 2019: doi: 10.1038/s41564-019-0602-7. #co-corresponding

Peterson ST*, Kennedy E*, Brigleb P, Taylor G, Urbanek K, Bricker T, Lee S, Shin H, Dermody T, Boon ACM, and Baldridge MT. Disruption of type III interferon genes Ifnl2 and Ifnl3 recapitulates loss of the type III IFN receptor in the mucosal antiviral response. Journal of Virology 2019: 93(22). * equal contribution

Ingle H*, Lee S*, Ai T, Orvedahl A, Rodgers R, Zhao G, Sullender M, Peterson ST, Locke M, Liu TC, Yokoyama CC, Sharp B, Schultz-Cherry S, Miner JJ, Baldridge MT. Viral complementation of immunodeficiency confers protection against enteric pathogens via interferon-λ. Nature Microbiology 2019: doi: 10.1038/s41564-019-0416-7. *equal contribution

Bennion BG, Ingle H, Ai TL, Miner CA, Platt DJ, Smith AM, Baldridge MT#, Miner JJ# (2019). A human gain-of-function STING mutation causes immunodeficiency and gammaherpesvirus-induced pulmonary fibrosis in mice. Journal of Virology. pii: JVI.01806-18. #co-corresponding

Wilen CB, Lee S, Hsieh LL, Orchard RC, Desai C, Hykes BL Jr, McAllaster MR, Balce DR, Feehley T, Brestoff JR, Hickey CA, Yokoyama CC, Wang YT, MacDuff DA, Kreamalmayer D, Howitt MR, Neil JA, Cadwell K, Allen PM, Handley SA, van Lookeren Campagne M, Baldridge MT, Virgin HW (2018). Tropism for tuft cells determines immune promotion of norovirus pathogenesis. Science. 360(6385):204-208.

Lee S, Wilen CB, Orvedahl A, McCune BT, Kim K, Orchard RC, Peterson ST, Nice TJ, Baldridge MT#, Virgin HW# (2017). Norovirus Cell Tropism is Determined by Combinatorial Action of a Viral Non-structural Protein and Host Cytokine. Cell Host & Microbe. 22(4):449-459. #co-corresponding

Moon C*, Baldridge MT*, Wallace MA, Burnham CD, Virgin HW, Stappenbeck TS. (2015). Vertically transmitted faecal IgA levels determine extra-chromosomal phenotypic variation. Nature, 521(7550):90-3. * equal contribution

Baldridge MT, Nice TJ, McCune BT, Yokoyama C, Kambal A, Wheadon M, Lazear HM, Diamond MS, Ivanova Y, Artyomov M, Virgin HW. (2015). Commensal microbes and interferon-λ determine persistence off enteric murine norovirus infection. Science, 347(6219):266-9.

Baldridge MT*, King KY*, Boles NC, Weksberg DC, and Goodell MA. Quiescent hematopoietic stem cells are activated by IFN-gamma in response to chronic infection. (2010). Nature, 465: 793-797. * denotes equal contribution

Last Updated: 4/1/2021 1:50:03 PM

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