Episomal replication of human papillomavirus type 16 from a cerv- vical carcinoma cell line CC7T

碩士 === 國立師範大學 === 生物學研究所 === 82 === Observing the replication of human papillomavirus is difficult because of lacking an in vitro system to support a stable episomal viral DNA replication. In 1980, Dr.C. P. Hu established a cerv...

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Bibliographic Details
Main Authors: Nien-Chen Huang, 黃念貞
Other Authors: Ming-Liang Lee
Format: Others
Language:zh-TW
Published: 1994
Online Access:http://ndltd.ncl.edu.tw/handle/69039474505063588037
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Summary:碩士 === 國立師範大學 === 生物學研究所 === 82 === Observing the replication of human papillomavirus is difficult because of lacking an in vitro system to support a stable episomal viral DNA replication. In 1980, Dr.C. P. Hu established a cervical carcinoma cell line CC7T, which contains both episomal and integrated HPV 16 DNA. Compare the DNA sequences with the prototype HPV 16 DNA, there are point mutations in both E1 andE7 ORFs in epi some, and these two genes are responsible for viral DNA replication. In order to prove whether these mutations could effect the existence of episomal DNA in CC7T, we transfected the cloned episome (pCC7T-BS) and the prototype HPV 16 DNA (pHPV-BS) into re lated cervical carcinoma and larynx carcinoma cell lines, HeLa and Hep-2, respectively. Our results showed that there were neither apparent changes in morphology nor cell death in transfected cells except pCC7T-BS transfected cell line HeLa. In HeLa , t wo days after transfection with pCC7T-BS , the growth of the cells delayed and the cells appeared to die 。 On the other hand , the replication patterns of both pCC7T-BS and pHPV-BS were similiar in HeLa and Hep-2. The amount of DNA were papillomavirus replication reduced gradually a Most of the informations about nd there were no apparent DNA replication in both cell lines. It indicated that the mutations occured in episome might not as important as we expected. come from researches of the bovine papillomavirus type 1.