Assistant Professor, Biomedical Sciences
- RSV, SARS-CoV-2, MERS, Ebola virus, Air-liquid interface 3D culture system, COPD, Host-pathogen interactions, Cytoskeletal dynamics, Cytoskeletal inflammation, Therapeutics and Vaccines.
Respiratory syncytial virus (RSV) is the leading cause of bronchiolitis (inflammation of lung’s airways) and pneumonia (inflammation of the lungs) in children younger than 5 years. There is currently no vaccine or cost-effective therapeutics against RSV infection. Studying RSV-host interactions in the human airway epithelium model will likely accelerate our understanding of RSV pathogenesis and potentially identifying novel strategies for limiting the severity of RSV-induced pathophysiology. The Mehedi lab research focuses on the host-pathogen interactions aspect of RSV infection. The lab uses normal human bronchial epithelial (NHBE) cells in an air-liquid interface 3D culture system to develop pseudo-stratified and fully differentiated mucociliary epithelium of healthy and COPD patients. For determining RSV-induced pathophysiology in this human airway epithelial model, the lab uses statute-of-the-art microscopy for determining cytoskeletal reorganization, SAVA system for determining the beat frequency of ciliated cells, EVOM2 for determining transepithelial electrical resistance, multiplex assays for determining cytokine and chemokines, and molecular biology techniques (qPCR, WB, IF, and IHC) for determining epithelial-mesenchymal transition. This RSV human airway epithelium model is useful for determining disease pathophysiology and identifying novel strategies to combat RSV infection. We previously identified actin-related protein 2 (ARP2) as a novel host factor for filopodia-driven RSV cell-to-cell spread— a novel cell-associated RSV spread mechanism. The lab research focuses on identifying novel anti-viral therapeutics by delineating the mechanism of filopodia-driven RSV spread. The lab research also focuses on RSV live-attenuated and mRNA-based vaccine development.
In response to the current global pandemic, the lab has also been studying the host-pathogen interactions aspect of SARS-CoV-2 infection in the in vitro lung epithelium models of healthy and COPD patients. The lab determines disparities in the pathophysiology of the lung infected with different coronaviruses (SARS-CoV, SARS-CoV-2, and MERS).
- Masfique Mehedi, Goblet Cells in SARS-CoV-2 Pathogenesis. 2020 - 11(1):102-104. AJBSR.MS.ID.001596.
- Osan J. K., S. K. Talukdar, F. Feldmann, B. A. DeMontigny, K. Jerome, K. L. Bailey, H. Feldmann, M. Mehedi. Goblet cell hyperplasia increases SARS-CoV-2 infection in COPD. bioRxiv. Preprint. 2020. Nov 12. 10.1101/2020.11.11.379099.
- Mehedi M., M. Smelkinson, J. Kabat, S. Ganesan, P.L. Collins, and U. J. Buchholz. Multicolor Stimulated Emission Depletion (STED) Microscopy to generate High-resolution Images of Respiratory Syncytial Virus Particles in Infected Cells. Bio-protocol, 2017, 7(17): e2543.
- Mehedi M., P.L. Collins, and U. J. Buchholz. A Novel Host Factor for Respiratory Syncytial Virus. Communicative & Integrative Biology, 2017, 10(3): e1319025.
- Le Nouen C., T. McCarty, M. Brown, M. Laird, R. Lleras, M. Dolan, M. Mehedi, L. Yang, S. Munir, J. M. DiNapoli, S. Mueller, E. Wimmer, P.L. Collins, and U. J. Buchholz. Genetic Stability of Genome-Scale Deoptimized RNA Virus Vaccine Candidates Under Selective Pressure. Proc Natl Acad Sci USA, 2017, 114(3): E386-E395.
- Mehedi M., T. McCarty, S.E. Martin, C. Le Nouën, E. Buehler, Y-C. Chen, M. Smelkinson, S. Ganesan, E. R Fischer, L.G. Brock, B. Liang, S. Munir, P.L. Collins, and U. J. Buchholz. Actin-Related Protein 2 (ARP2) and Virus- Induced Filopodia Facilitate Human Respiratory Syncytial Virus Spread. PLoS Pathog, 2016, 12(12): e1006062.
- Le Nouen C., L. G. Brock, C. Luongo, T. McCarty, L. Yang, M. Mehedi, E. Wimmer, S. Mueller, P. L. Collins, U. Buchholz, & J. N. DiNapoli. Attenuation of human respiratory syncytial virus by genome-scale codon-pair deoptimization. Proc Natl Acad Sci USA, 2014, 111(36): 13169-74.
- Mehedi M., T. Hoenen, T. Taylor, S. Ricklefs, M. Dolan, D. Falzarano, H. Ebihara, S. Porcella & H. Feldmann. Ebola virus RNA editing depends on the primary editing site sequence and an upstream secondary structure. PLoS Pathog, 2013, 9(10): e1003677.
- Grolla A., M. Mehedi, R. Lindsay, A. Duse, H. Feldmann. Molecular detection of Rift Valley fever virus is enhanced by testing whole blood. Journal of Clinical Virology, 2012. Vol 54 pp 313-317.
- Mehedi M., A. Groseth, H. Feldmann & H. Ebihara. Clinical aspects of Marburg hemorrhagic fever. Future Virology, 2011. Vol 6(9), pp 1091-1106.
- Mehedi M., D. Falzarano, J. Seebach, X.Hu, M. S. Carpenter, H. J. Schnittler, & H. Feldmann. A new Ebola virus nonstructural glycoprotein expressed through RNA editing. Journal of Virology, 2011. Vol 85(11), pp 5406-5414.
Ph.D. in Medical Microbiology, University of Manitoba, 2013
M.Sc. in Microbiology, University of Dhaka, 2005
B.Sc. in Biotechnology and Genetic Engineering, Khulna University, 2003