Correlation between ebv co-infection and HPV16 genome integrity in Tunisian cervical cancer patients

• Autor(a) principal: Kahla,Saloua
• Data de Publicação: 2012
• Outros Autores: Oueslati,Sarra, Achour,Mongia, Kochbati,Lotfi, Chanoufi,Mohamed Badis, Maalej,Mongi, Oueslati,Ridha
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Brazilian Journal of Microbiology
• Texto Completo: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1517-83822012000200039
• topic: Cervical cancer; Epstein-Barr virus; E2 gene; E2 mRNA; High risk human papillomaviruses

Infection with high risk Human papillomavirus (HR-HPV) is necessary but not sufficient to cause cervical carcinoma. This study explored whether multiple HR-HPV or coinfection with Epstein-Barr virus (EBV) influence the integration status of HPV16 genome. The presence and typing of HPV in a series of 125 cervical specimens were assessed by polymerase chain reaction (PCR) using the specific primers for the HPV L1 region. As for EBV infection, the viral EBNA1 gene was used for its detection through PCR amplification. Disruption of the HPV E2 gene was assessed by amplification of the entire E2 gene with single set of primers, while E2 transcripts were evaluated by a reverse transcription PCR method (RT-PCR). The overall prevalence of HPVDNA was of 81.8% in cervical cancers versus 26.9% in benign lesions. In HPV positive cases, HPV16 and HPV18 were the most prevalent types, followed by HPV types 33, 31. EBV EBNA1 prevalence was statistically more frequent in cervical carcinomas than in benign lesions (29.5%, vs 9.6%; P=0.01). No viral infection was detected in healthy control women. The uninterrupted E2 gene was correlated with the presence of E2 transcripts originating from the HPV episomal forms. It was observed that integration was more common in HPV18 and EBV coinfection. The presence of EBV caused a five-fold [OR= 5; CI= 1.15-21.8; P = 0.04] increase in the risk of HPV16 genome integration in the host genome. This study indicates that EBV infection is acting as a cofactor for induction of cervical cancer by favoring HPVDNA integration.