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BioMed Research International
Volume 2014, Article ID 639321, 8 pages
Research Article

Sequence Variation in the E2-Binding Domain of HPV16 and Biological Function Evaluation in Tunisian Cervical Cancers

1Unit of Immuno-Microbio-Environmental and Carcinogenesis (IMEC), Faculty of Sciences, University of Carthage, Jarzouna, 7021 Bizerta, Tunisia
2Radio-oncology Department, Salah Azaiz Institute, 1006 Tunis, Tunisia
3Research Laboratory of Antimicrobial Resistance, Faculty of Medicine of Tunis, 1007 Tunis, Tunisia
4Service of Gynaecology Obstetrics A, Center of Maternity and Neonatology, Hospital La Rabta, 1007 Tunis, Tunisia

Received 19 February 2014; Revised 22 May 2014; Accepted 30 May 2014; Published 17 June 2014

Academic Editor: Anton M. Jetten

Copyright © 2014 Saloua Kahla et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


HPV16 E2 variants have different effects on the transcriptional activity of the LCR. In this study, we examined the nucleotide and amino acid sequence variation within the HPV16 E2 gene and to correlate with disease progression. E2 gene disruption was detected by PCR amplification of the entire E2 gene using a single set of primers. Nucleotide variations were analyzed by bidirectional sequencing. mRNA expression patterns of E6 and E7 gene transcripts were evaluated by a reverse transcriptase-PCR method (RT-PCR). The detection of intact E2 genes was significantly higher among controls than cases (81.8% versus 37.5%, resp., ). Among the E subgroup, variation at position 3684 C>A results in the amino acid substitution T310K and was more common among the E2 undisrupted cases (7/9; 77.7%), compared to controls (2/9; 22.2%). In addition, specific sequence variations identified in the E2 ORF at positions 3684 C>A were associated with increased viral oncogenes E6-E7 production. Besides HPV16 E2 disruption, the 3684 C>A variation within undisrupted E2 genes could be involved in an alternative mechanism for deregulating the expression of the HPV16 E6 and E7 oncogenes and appears to be a major factor contributing to the development of cervical cancer in Tunisian women.