Changes in the physical state and expression of human papillomavirus type 16 in the progression of cervical intraepithelial neoplasia lesions analysed by PCR

• Published in: Journal of general virology Vol. 76; no. 10; pp. 2589 - 2593
• Main Authors: Daniel, Betty, Mukherjee, Geetasree, Seshadri, Lakshmi, Vallikad, Elizabeth, Krishna, Sudhir
• Format: Journal Article
• Language: English
• Published: England Soc General Microbiol 01.10.1995
• Subjects: Cervical Intraepithelial Neoplasia - pathology; Cervical Intraepithelial Neoplasia - virology; DNA Primers; DNA, Viral - analysis; DNA-Binding Proteins; Female; Gene Expression Regulation, Viral; Genes, Viral - genetics; Humans; Oncogene Proteins, Viral - genetics; Papillomaviridae - genetics; Papillomaviridae - isolation & purification; Papillomaviridae - physiology; Plasmids - analysis; Polymerase Chain Reaction - methods; Repressor Proteins; Uterine Cervical Neoplasms - pathology; Uterine Cervical Neoplasms - virology; Virus Integration
• ISSN: 0022-1317; 1465-2099
• DOI: 10.1099/0022-1317-76-10-2589

1 National Centre for Biological Sciences, Tata Institute of Fundamental Research, PO Box 1234, Bangalore 560012 2 Department of Obstetrics and Gynaecology, Christian Medical College, Vellore and 3 Department of Pathology and 4 Department of Gynaecology, Kidwai Institute of Oncology, Bangalore 560029, India Using a PCR strategy which detects disruptions in the E2 reading frame we have analysed the progression of human papillomavirus type 16 (HPV-16)-positive cervical lesions. From a total of 192 samples analysed, we detected HPV-16 in 74. In samples from the spectrum of inflammatory states and cervical intraepithelial neoplasia (CIN) grade I lesions we detected episomal forms of the virus. In invasive tumours and in samples from CIN III lesions there were no episomes detected, suggesting that lesions with integrated HPV-16 precede the invasive stage. The RT-PCR analysis demonstrated the presence of E6 transcripts at all stages and E2 transcripts in all early lesions. The E2 transcripts were not detected in 26 out of 29 CIN III lesions and tumours in which there was a disruption in the E2 gene. In tumours with E2 gene disruptions, we used single-primer PCR to demonstrate the presence of E2 gene sequences. * Author for correspondence. Fax +91 80 3343851. e-mail betty@tifrbng.ernet.in Received 21 March 1995; accepted 18 May 1995.