Hepatitis B virus (HBV) is the most prevalent human tumor virus and causes most virus-associated human cancers. It is estimated that chronic HBV infection cause 500,000 causes of live cancer annually. HBV must actively replicate within liver cells to maintain its chronic infection. Dr. Loeb and colleagues work to understand how HBV carries out the individual steps by which it replicates its genome in order to understand how this virus contributes to human cancer. HBV replicates its genome by a reverse transcription pathway, which involves switching templates three times during the course of DNA synthesis. Dr. Loeb and colleagues will pursue several complementary goals to understand the mechanisms of each of the three templates switches that are required for genome replication of HBV. First, they will define the cis-acting elements of the nucleic acid template required for each of the three template switches. Concomitant with these analyses, they will characterize the ability of viruses with mutations within these cis-actin sequences to carry out the relevant template switch, with the goal of gaining insights into mechanisms underlying these switches. Lastly, they will identify other viral components, either nucleic acid or protein, that are specifically involved with each of the template switches, using complementary approaches.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Research Program Projects (P01)
Project #
3P01CA022443-24S1
Application #
6502902
Study Section
Project Start
2001-05-01
Project End
2002-04-30
Budget Start
Budget End
Support Year
24
Fiscal Year
2001
Total Cost
$183,401
Indirect Cost
Name
University of Wisconsin Madison
Department
Type
DUNS #
161202122
City
Madison
State
WI
Country
United States
Zip Code
53715
Weng, Chao; Lee, Denis; Gelbmann, Christopher B et al. (2018) Human Cytomegalovirus Productively Replicates In Vitro in Undifferentiated Oral Epithelial Cells. J Virol 92:
Bristol, Jillian A; Djavadian, Reza; Albright, Emily R et al. (2018) A cancer-associated Epstein-Barr virus BZLF1 promoter variant enhances lytic infection. PLoS Pathog 14:e1007179
Romero-Masters, James C; Ohashi, Makoto; Djavadian, Reza et al. (2018) An EBNA3C-deleted Epstein-Barr virus (EBV) mutant causes B-cell lymphomas with delayed onset in a cord blood-humanized mouse model. PLoS Pathog 14:e1007221
UmaƱa, Angie C; Iwahori, Satoko; Kalejta, Robert F (2018) Direct Substrate Identification with an Analog Sensitive (AS) Viral Cyclin-Dependent Kinase (v-Cdk). ACS Chem Biol 13:189-199
Meyers, Jordan M; Grace, Miranda; Uberoi, Aayushi et al. (2018) Inhibition of TGF-? and NOTCH Signaling by Cutaneous Papillomaviruses. Front Microbiol 9:389
Uberoi, Aayushi; Yoshida, Satoshi; Lambert, Paul F (2018) Development of an in vivo infection model to study Mouse papillomavirus-1 (MmuPV1). J Virol Methods 253:11-17
Djavadian, Reza; Hayes, Mitchell; Johannsen, Eric (2018) CAGE-seq analysis of Epstein-Barr virus lytic gene transcription: 3 kinetic classes from 2 mechanisms. PLoS Pathog 14:e1007114
Chakravorty, Adityarup; Sugden, Bill (2018) Long-distance communication: Looping of human papillomavirus genomes regulates expression of viral oncogenes. PLoS Biol 16:e3000062
Chiu, Ya-Fang; Sugden, Bill (2018) Plasmid Partitioning by Human Tumor Viruses. J Virol 92:
Shin, Myeong-Kyun; Payne, Susan N; Bilger, Andrea et al. (2018) Activating Mutations in Pik3caContribute to Anal Carcinogenesis in the Presence or Absence of HPV-16 Oncogenes. Clin Cancer Res :

Showing the most recent 10 out of 434 publications