Cervical cancer is the second most prevalent cancer among the Algerian women. The association between human papilomavirus (HPV) and cervical neoplasia is well documented . High risk oncogenic HPV types (including HPV 16 and HPV 18) are associated with 99.7% of all low-grade cervical (CIN-1 or mild CIN) and high grade intraepithelial lesions (CIN-2/3) and hence, they play an important role in cervical cancer development. Now, and since 1976, it is well recognized that HPV infections in the cervix are frequently associated with intraepithelial neoplasia and invasive squamous cell carcinomas (SCC) with all their different histological variants (large-cell keratinizing, large-cell non-keratinizing and small-cell carcinoma).
The long period of time (years) it takes for the development of cervical cancer after HPV infection suggests the involvement of other etiologies (such as viruses or cell compounds) in malignancy process. The synergistic effect of carcinogenic factors such as two or more viruses interacting at different stages of tumor development has been reported [2–4]. Epstein-Barr virus (EBV), ubiquitous human gamma-herpes virus responsible for mononucleosis , could be one of the ‘helper’ viruses. It can be sexually transmitted  and replicates in cervix cells . EBV infection, widely spread among the population [7, 8], has been associated with an increasing number of lymphocytic and epithelial cancers, mainly Burkitt’s lymphoma, Hodgkin’s lymphoma, T cell lymphoma, nasopharyngeal carcinoma (NPC) and gastric adenocarcinoma [9, 10].
BARF1 is one of the EBV-encoded proteins secreted in the serum of NPC patients  and expressed in more than 90% of NPC biopsies [12–15] and tumor epithelial cells of EBV-associated gastric carcinoma . It has a malignant transforming activity in rodent fibroblasts  and in EBV-negative human B cells . LMP1, another EBV oncogene candidate essential for B cell immortalization , was present in 30 to 50% of NPC biopsies . This oncogene can activate a number of cellular key genes such as NFκB and EGFR [17, 19]. LMP-1 can inhibit cell differentiation when transfected into epithelial cells .
Tseng et al.  reported a high incidence of EBV in lymphoepithelial like-carcinoma (LELC) patients but did not show any association with HPV. These findings are in contradiction with what has been previously reported [21, 22]. Therefore, the oncogenic relationship between the two viruses remains not fully understood. Added to this, the presence of EBV in the cervix carcinoma remains equally a topic of great debate among virologists, confirmed by certain authors [2, 23, 24] but not by others [25, 26].
As it is well known EBV can transform cells bearing the EBV/C3d receptor making them receptive to other oncogenic stimuli . These receptors are widely detected on ecto- and endo-cervical biopsies of the uterine cervix [28–30]. EBV replicates in cervical epithelium and its possible role in cervical carcinoma development has been raised.
We looked, in this study, for the presence of both EBV and HPV DNA sequences in Algerian patients with SCC and cervical lesions. We examined the presence of EBV infection and the EBV-HPV co-infection. The presence of EBV in cervical cancer tissues suggests its possible involvement in the cervical cancer progression. Initially, PCR amplification was used to identify the co-infection. This was followed by an investigation on EBV oncogenes (BARF-1, LMP-1 and EBNA-1) expression using immunoblotting and immunohistochemistry. This expression would reflect the transformation mechanism of cervical cells.
Since EBV could play an important role in Nasopharyngeal carcinoma and Burkitt’s lymphoma highly frequent in Algeria, Our hypothesis was a possible co-infection by HPV and EBV in Algerian SCC and cervical lesions.