Biology Faculty Articles
Title
HSV-2-induced Tumorigenicity in HPV 16-immortalized Human Genital Keratinocytes
Document Type
Article
Publication Date
8-1990
Publication Title
Virology
Keywords
Carcinoma, Squamous cell/microbiology, Carcinoma squamous cell/pathology, Cell transformation neoplastic, Cells cultured, DNA viral/genetics, Epithelial cells, Female, Genes viral, Humans, Keratinocytes/cytology, Papillomaviridae/genetics, Simplexvirus/genetics, Transfection, Uterine cervical neoplasms/microbiology, Uterine cervical neoplasms/pathology
ISSN
0042-6822
Volume
177
Issue/No.
2
First Page
777
Last Page
779
Abstract
A subgenomic region of HSV-2, BglII N, is capable of converting immortal genital epithelial cells containing integrated HPV16 sequences into tumorigenic squamous cell carcinoma cells. Moreover, tumor-derived cultured cells and immortal cells that had been transfected with HSV-2/BglII N and kept in continuous culture subsequently lost the HSV-2 sequences. The HSV-2/Bg/II N sequence was ineffective on normal cells. Thus, HSV-2/Bg/II N may act as a cofactor in the genesis of a carcinoma but is not required to maintain the transformed phenotype. Although pa pillornaviruses (HPVs) are currently receiving much attention because of their association with cervical squamous carcinomas, ample reasons exist to suggest a multifactorial etiology in which additional factors are necessary to convert dysplastic lesions to carcinomas. The hypothesis that specific HPV types may be necessary but not sufficient to cause cancer is reinforced. Thus, HSV-2-transforming sequences have a potential role in the etiology of human cervical cancer.
NSUWorks Citation
Dipaolo, Joseph A.; Craig D. Woodworth; Nicholas C. Popescu; Debra L. Koval; Jose V. Lopez; and Jay Doniger. 1990. "HSV-2-induced Tumorigenicity in HPV 16-immortalized Human Genital Keratinocytes." Virology 177, (2): 777-779. doi:10.1016/0042-6822(90)90548-6.
ORCID ID
0000-0002-1637-4125
ResearcherID
F-8809-2011
DOI
10.1016/0042-6822(90)90548-6
Comments
©1990 Elsevier Inc.