1991 Fiscal Year Final Research Report Summary
Interaction between Human Papillomaviruses and Keratinization
| Project/Area Number |
01570578
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Dermatology
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| Research Institution | The Jikei University School of Medicine |
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Principal Investigator |
HONDA Mariko The Jikel University School of Medicinet, Lecturer, 医学部, 講師 (20100919)
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| Co-Investigator(Kenkyū-buntansha) |
MINESAKI Yukinori The Jikei University School of Medicinet, Assistant, 医学部, 助手 (40229779)
YOKOI Kiyoshi The Jikei University School of Medicinet, Assistant, 医学部, 助手 (70182681)
ISHIDA Takashim The Jikei University School of Medicinet, Assistant, 医学部, 助手 (90159731)
NIIMURA Michihito The Jikei University School of Medicinet, Professor, 医学部, 教授 (00010190)
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| Project Period (FY) |
1989 – 1991
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| Keywords | human papillomavirus / keratinization / Myrmecia / condyloma acuminatum / early gene / late gene / in situ hybridization |
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| Research Abstract |
Human papillomaviruses (HPV) infect and replicate in keratinocytes, inducing benign skin tumors. The migration of keratinocytes from the basal layer to the upper layers of the epidermis and their associated squamous differentiation is accompanied by changes in the cellular environment that apparently promote the replication of the viral DNA to detectable levels and the expression of viral proteins. In this study we investigated the HPV-keratinocyte interaction.
Using in situ hybridization, we detected the mRNA of the late genes of HPV which code for the viral structural proteins in the cells of the spinous layer, but the mRNA was not detectable in the basal cells and cultured wart cells. We also detected the mRNA of the early genes which control DNA replication and transform the host cells in the basal cells and cultured warts cells. No HPVmRNA was detected in the HPVDNA transfected cells. The p53 tumor suppressor genes were not abnormally expressed in the warts.
In near future we will attempt to detect proteins in keratinocytes which bind to HPV promoters, and proteins from HPV which bind to promoters of keratinocyte genes.
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