The Epstein-Barr virus (EBV) is highly penetrant in AIDS-associated non-Hodgkin's lymphomas where it is a key driver of the tumor phenotype. While EBV latency genes are critical for facilitating the tumor phenotype, the switch from latency to the lytic cycle is a critical aspect of a successful EBV infection program. As a result, the mechanisms driving this switch have been topics of active investigation over the years. Although EBV reactivation can be achieved in tissue culture through stimulation of the B-cell receptor (with anti-Ig) or the TGF-beta receptor (with ectopic TGF-beta), it is uncertain how common such events are in EBV-infected lymphocytes in vivo (work from David Thorley-Lawson's lab). The overarching hypothesis of this application is that EBV has evolved with a sensing mechanism for latently infected B-cells to detect when they encounter an epithelial cell environment. This model proposes that environmental cues from the oral/tonsil epithelium (in the late stages of the germinal center reaction, for example) trigger reactivation in B-cells, thereby facilitating the B-cell to epithelial cell viral transfer that is a fundamental first step n oral epithelial plaque formation and host- to-host transmission.

Public Health Relevance

The EBV infection cascade involves a complex series of events. A critical component of host-to-host transmission is the transfer of virus from B-cells harboring the latency viral reservoir to the oral epithelium where infectious virus is amplified an secreted into the saliva. We hypothesize that this transfer is orchestrated, in part, through cell o cell communication between epithelial cells and latently infected B-cells to increase the efficiency of this exchange pathway.

National Institute of Health (NIH)
National Institute of Allergy and Infectious Diseases (NIAID)
Research Project (R01)
Project #
Application #
Study Section
Special Emphasis Panel (ZRG1)
Program Officer
Beisel, Christopher E
Project Start
Project End
Budget Start
Budget End
Support Year
Fiscal Year
Total Cost
Indirect Cost
Tulane University
Schools of Medicine
New Orleans
United States
Zip Code
Zhang, Jinqiang; Baddoo, Melody; Han, Chang et al. (2016) Gene network analysis reveals a novel 22-gene signature of carbon metabolism in hepatocellular carcinoma. Oncotarget :
Liu, Yao-Zhong; Maney, Pooja; Puri, Jyoti et al. (2016) RNA-sequencing study of peripheral blood monocytes in chronic periodontitis. Gene 581:152-60
Zhang, Wensheng; Edwards, Andrea; Fang, Zhide et al. (2016) Integrative Genomics and Transcriptomics Analysis Reveals Potential Mechanisms for Favorable Prognosis of Patients with HPV-Positive Head and Neck Carcinomas. Sci Rep 6:24927
O'Grady, Tina; Wang, Xia; Höner Zu Bentrup, Kerstin et al. (2016) Global transcript structure resolution of high gene density genomes through multi-platform data integration. Nucleic Acids Res 44:e145
Liu, Yao-Zhong; Roy-Engel, Astrid M; Baddoo, Melody C et al. (2016) The impact of oil spill to lung health--Insights from an RNA-seq study of human airway epithelial cells. Gene 578:38-51
Yin, Qinyan; Wang, Xia; Roberts, Claire et al. (2016) Methylation status and AP1 elements are involved in EBV-mediated miR-155 expression in EBV positive lymphoma cells. Virology 494:158-67
Zhou, Xiang; Hao, Qian; Liao, Peng et al. (2016) Nerve growth factor receptor negates the tumor suppressor p53 as a feedback regulator. Elife 5:
Zhan, Yang; Zhang, Guanyi; Wang, Xiaojie et al. (2016) Interplay Between Cytoplasmic and Nuclear Androgen Receptor Splice Variants Mediate Castration Resistance. Mol Cancer Res :
Lin, Zhen; Swan, Kenneth; Zhang, Xin et al. (2016) Secreted Oral Epithelial Cell Membrane Vesicles Induce Epstein-Barr Virus Reactivation in Latently Infected B Cells. J Virol 90:3469-79
Deininger, Prescott; Morales, Maria E; White, Travis B et al. (2016) A comprehensive approach to expression of L1 loci. Nucleic Acids Res :

Showing the most recent 10 out of 47 publications