HPV expression, implicating HSV as a possible co- 
factor in HPV-induced disease. In addition, the 
phorbol ester 12-0-tetradecanoylphorbol-13-ace- 
tate (TPA) also has been shown to increase HPV-18 
expression, suggesting chemical cofactors also may 
act to alter papillomavirus transcription. 
III. Transgenic Models for HPV-16- and HPV-18- 
Induced Disease. 
A series of HPV-16 and HPV-18 transgenic mice 
have been constructed, in collaboration with Dr. 
Robert E. Hammer (HHMI, University of Texas 
PUBLICATIONS 
Southwestern Medical Center at Dallas), in an at- 
tempt to show a causal relationship between HPV 
and epithelial tumors. After 10 months, 25% of 
male founder mice expressing the E6-E7 region 
alone, developed hyperplastic seminal vesicles. This 
phenotype has been transmitted through the 
germline and appears to be linked to expression of 
the E6-E7 region of HPV-18. 
Dr. Laimins is also Assistant Professor of Molecu- 
lar Genetics and Cell Biology and on the Commit- 
tee on Virology at The University of Chicago. 
Articles 
Bedell, M.A., Jones, K.H., Grossman, S.R., and Laimins, L.A. 1989. Identification of human papillomavirus 
type 18 transforming genes in immortalized and primary cells. J Virol 63:1247-1255. 
Gius, D., and Laimins, L.A. 1989. Activation of human papillomavirus type 18 gene expression by herpes sim- 
plex virus type 1 viral transactivators and a phorbol ester. J Virol 63:555-563. 
Grossman, S.R., Mora, R., and Laimins, L.A. 1989. Intracellular localization and DNA-binding properties of 
human papillomavirus type 18 E6 protein expressed with a baculovirus vector. J Virol 63:366-374. 
McCance, D.J., Kopan, R., Fuchs, E., and Laimins, L.A. 1988. Human papillomavirus type 16 alters human epi- 
thelial cell differentiation in vitro. Proc Natl Acad Sci USA 85:7169-7173. 
236 
