Jason M. Bodily, Ph.D

Assistant Professor                                                                                                                

Contact Information:

Email: jbodil@lsuhsc.edu
Office Phone: 318-675-4890                             
Laboratory Phone: 318-675-4862
Office Fax: 318-675-5764

Education/Training:

Postdoctoral Study, Northwestern University School of Medicine

Ph.D., Microbiology, 2005, Penn State College of Medicine

M.S., Microbiology, 2000, Brigham Young University

B.S., Molecular Biology, 1999, Brigham Young University

Major Research Interests:

Human papillomavirus pathogenesis,
viral-host interactions, viral oncogenesis

Human papillomaviruses (HPVs) are the causative agents of cervical and other cancers.  As part of their normal life cycles, these small DNA viruses infect stratified epithelia and establish persistent infections, usually resulting in minor hyperproliferation, but occasionally progressing to malignancy.  My interest is in the viral-host interactions that enable HPVs to persist and multiply.  We can model all phases of the viral life with both wild-type and genetically modified viruses using a variety of cell culture techniques, including organotypic culture, to establish persistent HPV infections in vitro.  Major life cycle events, functions of viral and host genes, and the host cell response to infection are studied using the techniques of molecular biology.  Current focus in the laboratory is on the interaction of cellular and viral regulatory proteins to control viral and cellular gene expression, how viral manipulation of cellular genes affects interaction between infected epithelia and neighboring stroma, and how these changes lay the groundwork for cancer development.  

Representative Publications:

JM Bodily, M Nakamura, M. Beglin, S Kyo, M Inoue, LA Laimins. Hypoxia-specific stabilization of HIF-1α by human papillomaviruses.  Virology, 387(2):442-8, 2009. 

JM Bodily, KPM Mehta, and LA Laimins.  Human papillomavirus E7 enhances hypoxia inducible factor-1 mediated transcription by inhibiting binding of histone deacetylases.  Cancer Research 71:1187-95, 2011.


JM Bodily, KPM Mehta, L Cruz, C Meyers, and LA Laimins.  The E7 open reading frame acts in cis and trans to mediate differentiation-dependent activities in the human papillomavirus type 16 life cycle, Journal of Virology, 85(17):8852-62, 2011.

JM Bodily, GA Wrobel, C Hennigan, and CM Rodriguez. Regulation of the human papillomavirus type 16 late promoter by E7 and the cell cycle. Virology 433(1):11–19, 2013 (Featured in Virology Highlights Blog)

EJ Gauson, MM Donaldson, ES Doran, X Wang, M Bristol, JM Bodily, and IM Morgan. Evidence supporting a role for TopBP1 and Brd4 in the initiation but not continuation of human papillomavirus 16 E1/E2 mediated DNA replication. Journal of Virology, 1;89(9):4980-91, 2015

E Langsfield, JM Bodily, and LA Laimins. The deacetylase Sirtuin 1 regulates human papillomavirus replication by modulating histone acetylation and recruitment of DNA damage factors NBS1 and Rad51 to viral genomes. PLoS Pathogens, 2015 Sep 25;11(9):e1005181. doi: 10.1371/journal.ppat.1005181, 2015

T Klymenko, H Hernandez-Lopez, A MacDonald, JM Bodily, and S Graham. Human papillomavirus E2 regulates SRSF3 (SRp20) to promote capsid protein expression in infected differentiated keratinocytes. J. Virol. 90(10):5047-5058, 2016 (Spotlighted as an Article of Significant Interest)

All Publications: Pubmed