[Analysis of the relative distribution and gene variation of HPV16 transforming gene at different stages of cervical lesions].
OBJECTIVE
The aim of this study was to analyze the relative distribution and gene variation of HPV16 transforming gene E6, E7 and E5 at different stages of cervical lesions.


METHODS
DNA was extracted from tissue samples of 200 patients with cervical lesions, including 124 cervical cancer, 17 CIN grade I and II, 23 CIN grade III and 36 cervicitis. Then HPV16 E6, E7 and E5 genes were amplified, and part of the E6 and E7 PCR products were sequenced using the HPV16 E6 and E7 specific primers.


RESULTS
The positive rate of E6 gene in cervicitis, CINI and CINII, CINIII and cervical cancer was 25.0%, 29.4%, 60.9% and 76.6%, respectively. The positive rate of E7 gene was 16.7%, 41.2%, 43.5% and 61.3%, respectively. The positive rate of E5 gene was 5.6%, 5.9%, 30.4% and 40.3%, respectively. HPV16 E6 gene mutations in Nt 178 were found in 47 case from 80 cervical cancer samples, resulting in amino acid change of Asp to Glu. The mutation rate was 58.8%.Otherwise the mutation rate of E6 178 in cervicitis and CIN I approximately III samples was 25.0% and 31.8%. E7 mutations were found in Nt 647 in 21 cervical samples from 30 cervical cancer samples, resulting in amino acid change of Asn to Ser. The mutation rate was 70.0%. The mutation rate of E6 647 in cervicitis and CINI approximately III samples was 35.0% and 40.9%, respectively.


CONCLUSIONS
The positive rate of E6 and E7 increase gradually from cervicitis, CINI and CINII, CINIII to cervical cancer. The rate of E5 is relatively lower than that of E6 and E7 gene in cervical tissue samples. These results show that E6 and E7 gene are highly associated with the progress of cervical cancer and E5 genes are lost in the development of cervical cancer. High frequency mutations of HPV16 E6 and E7 gene in E6 178, E7 647 have been found in cervical cancer samples in Hubei province, China. These results approved that the HPV16 variants prevalent in this area are different from the European and African variants.
Zhang
Fan
F
Department of Gynecologic Oncology, Zhongnan Hospital, Wuhan University, China.
Ding
Xiao-hua
XH
Cai
Hong-bing
HB
Wang
Hua
H
Chen
Chang-chun
CC
Zhang
Shuai
S
D000328:Adult; D002277:Carcinoma / Q000378:metabolism / Q000821:virology*; D002681:China; D005260:Female; D052162:Human papillomavirus 16 / Q000235:genetics*; D006801:Humans; D008875:Middle Aged; D009856:Oncogene Proteins, Viral / Q000235:genetics* / Q000378:metabolism; D050725:Papillomavirus E7 Proteins / Q000235:genetics / Q000378:metabolism; D030361:Papillomavirus Infections / Q000235:genetics; D017354:Point Mutation; D012097:Repressor Proteins / Q000235:genetics / Q000378:metabolism; D002583:Uterine Cervical Neoplasms / Q000378:metabolism / Q000821:virology*; D002575:Uterine Cervicitis / Q000378:metabolism / Q000821:virology; D002578:Uterine Cervical Dysplasia / Q000378:metabolism / Q000821:virology; D000086082:Viroporin Proteins
D009856:Oncogene Proteins, Viral; D050725:Papillomavirus E7 Proteins; D012097:Repressor Proteins; C068651:E6 protein, Human papillomavirus type 16; C054859:oncogene protein E5, Human papillomavirus type 16; D000086082:Viroporin Proteins; C059731:oncogene protein E7, Human papillomavirus type 16