Mingyu Ding Professor of Microbiology and Immunology and Interim Department Head
Office Phone: 318-675-5760
Laboratory Phone: 318-675-5761
Office Fax: 318-675-5764
Postdoctoral Study, University of Rochester
Ph.D., Molecular Genetics, 1987 University of Konstanz
M.S. (Diplom), Molecular Genetics, 1984, University of Konstanz
B.S. (Vordiplom), Biology, 1981, University of Konstanz
Virus cell interactions, molecular pathogenesis of oncogenic human papillomaviruses
Certain types of human papillomaviruses (HPV) are the major cause of virus-induced malignancies in the human, like cervical carcinoma, the second most common cancer in women worldwide, and a subset of oropharyngeal squamous cell carcinoma (OSCC). Papillomaviruses are non-enveloped DNA viruses, which exclusively replicate in the skin and mucosa. Due to the dependence on terminally differentiating tissues for their propagation, the study of the papillomavirus life cycle has been hampered. The development of surrogate systems for the generation of papillomaviruses in recent years has allowed us to investigate processes involved in virus binding, uptake, and intracellular transport. More recently, we developed a novel cell culture model that allows highly efficient infection of primary keratinocytes and thus the complete HPV life cycle but especially immediate early events following infectious delivery of HPV genomes.
Sapp, M.J. (2013) HPV virions hitchhike a ride on retromer complexes. PNAS 110:7116-7.
Richards, K.F., Bienkowska-Haba, M., Dasgupta, J., Chen, X. S., and Sapp, M. (2013): Multiple heparan sulfate binding site engagements are required for the infectious entry of human papillomavirus type 16. J Virol 87:11426-37.
DiGiuseppe S, Keiffer TR, Bienkowska-Haba M, Luszczek W, Guion LGM, and Sapp M. (2015): The topography of HPV16 L2 protein in intracellular membranes following infectious entry. J Virol 89: 10442-52.
DiGiuseppe S, Luszczek W, Keiffer TR, Bienkowska-Haba M, Guion LGM, and Sapp M. (2016): Incoming HPV16 genome resides in a vesicular compartment throughout mitosis. PNAS 113(22):6289-94
Bienkowska-Haba M, Luszczek W, Keiffer TR, Guion LGM, DiGiuseppe S, Scott RS, and Sapp M (2016): PML protein protects viral genome from degradation after human papillomavirus type 16 infections. Cell Microbiol doi: 10.1111/cmi. 12708
DiGiuseppe S, Bienkowska-Haba M, Guion LGM, Keiffer TR, Sapp M. Human papillomavirus major capsid protein L1 remains associated with the incoming viral genome throughout the entry process. J Virol. 2017. Epub 2017/06/02. doi: 10.1128/jvi.00537-17. PubMed Central PMCID: PMC5533910. (featured in spotlight section).
Bienkowska-Haba M, Luszczek W, Myers JE, Keiffer TR, DiGiuseppe S, Polk P, et al. A new cell culture model to genetically dissect the complete human papillomavirus life cycle. PLoS Pathog. 2018;14(3):e1006846. Epub 2018.
All Publications: PubMed