NIH Independent Research Scholar
Established in 2019
Carrie Mae Long, Ph.D. (She/Her/Hers)
Independent Research Scholar
Major Areas of Research
- Coxiella burnetii, the causative agent of Q fever
- Identification of host and bacterial factors involved in C. burnetii virulence
- Development of a safe and effective Q fever vaccine
- Characterization of post-vaccination hypersensitivity responses
Coxiella burnetii is a highly infectious, zoonotic bacterial pathogen that causes a potentially debilitating febrile illness in humans called Q fever. C. burnetii is remarkably environmentally stable and typically causes Q fever via aerosol transmission. Bacterial pathogens with these attributes pose a threat to human health both due to potential bioterrorism and incidental exposure. Indeed, in 2007 a Q fever outbreak occurred in the Netherlands, resulting in nearly 4,000 human cases. This outbreak demonstrated the human health burden and the economic losses that can result from this disease, which is endemic worldwide.
Our group seeks to gain a better understanding of bacterial and host factors involved in C. burnetii virulence. Additionally, we are focused on developing a “better” Q fever vaccine. The current Q fever vaccine is highly efficacious but can cause a post-vaccination hypersensitivity (PVH) response; thus, the vaccine is not widely deployed. We seek to understand the immunologic mechanisms underlying vaccine-mediated protection and the PVH response. We primarily use in vivo models of disease and bacterial genetic manipulation to achieve these research goals. Currently, we are expanding the guinea pig model, which serves as the superior small animal model for Q fever. Ultimately, our research goals are aimed at understanding the host-pathogen relationship between humans and C. burnetii, which may lead to the development of novel preventative measures for Q fever.
Ph.D., 2016, West Virginia University
B.S., 2011, Gardner-Webb University
Dr. Long graduated summa cum laude from Gardner-Webb University with a B.S. in 2011. She received her Ph.D. in immunology and microbial pathogenesis from West Virginia University in 2016. Here, she studied the role of regulatory T cells and microRNAs in chemical allergy at the National Institute for Occupational Safety and Health (CDC). After earning her doctorate, Dr. Long moved to Hamilton, Montana, to join Dr. Robert Heinzen’s group at the National Institutes of Health to work as an Intramural Research Training Award postdoctoral fellow. During this time, Dr. Long worked in the biosafety level 3 laboratory researching the causative agent of Q fever, Coxiella burnetii. She investigated both bacterial and host factors required for virulence and refined guinea pig models for infection, vaccination, and post-vaccination hypersensitivity. In 2019, Dr. Long received an Independent Research Scholar Award from NIH, allowing her to form an autonomous research group to continue her work on Coxiella burnetii.
Binette P, Tesfamariam M, Cockrell D, Heinzen R, Richards C, Shaia C, Long CM. Murine Q fever vaccination model reveals sex dimorphism in early phase delayed-type hypersensitivity responses. Frontiers in Immunology. 2022. Accepted
Tesfamariam M, Binette P, Long CM. Preclinical Animal Models for Q Fever Vaccine Development. Front Cell Infect Microbiol. 2022 Feb 10;12:828784.
Long CM, Marzi A. Biodefence research two decades on: worth the investment? Lancet Infect Dis. 2021 Aug;21(8):e222-e233.
Long CM, Beare PA, Cockrell DC, Fintzi J, Tesfamariam M, Shaia CI, Heinzen RA. Contributions of lipopolysaccharide and the type IVB secretion system to Coxiella burnetii vaccine efficacy and reactogenicity. NPJ Vaccines. 2021 Mar 19;6(1):38.
Long CM, Beare PA, Cockrell DC, Larson CL, Heinzen RA. Comparative virulence of diverse Coxiella burnetii strains v. Virulence. 2019 Dec;10(1):133-150. doi: 10.1080/21505594.2019.1575715. PMID: 30782062; PMCID: PMC6389282.
Beare PA, Jeffrey BM, Long CM, Martens CM, Heinzen RA. Genetic mechanisms of Coxiella burnetii lipopolysaccharide phase variation. PLoS Pathog. 2018 Feb 26;14(3):e1006922.
Our work involves the study of bacterial-host interactions using relevant cellular and animal model systems. We seek to elucidate immunologic mechanisms involved in these interactions and use this knowledge to advance preclinical therapeutic and vaccine development efforts.