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.

Results obtained in the present work indicated that the Luminex assay is more sensitive than ELISA. The reactivity to the early antigens E6 and E7 was 37% versus 42% for HPV 16 and 21% versus 20% for HPV 18 among cervical cancer cases using ELISA. However, these ratios were 44% and 61%, respectively, for E6 and E7 HPV 16 versus 28% and 21% for E6 and E7 HPV 18 when using the Luminex technique. Data also indicated that HPV 16 and HPV 18 showed distinct profiles for the different antigens tested. Finally, the differences in antibody responses between cervical cancer cases and benign cases toward the different antigens were significant.

The aim of the present work was to study the immune profiling of prostate epithelial cells by the expression of ASK‐1/p38 and Raf‐1/ERK MAP Kinases signaling pathways mediated by TRAF‐6. Immunohistochemical and Western blot analyses for TRAF‐6, ASK‐1, MEK‐6, p38, Raf‐1, MEK‐1, ERK‐1, ERK‐2 and PSA were carried out in 5 samples of normal prostate gland, 24 samples of BPH and 19 samples of PC. Immunoreaction to TRAF‐6 was found in the cytoplasm of epithelial cells of BPH and tumor cells of PC samples. For patients with the profile (TRAF‐6+), optical densities revealed a weak immunoexpression of ASK‐1 in PC compared to BPH patients. Whereas, immunoexpression to Raf‐1 was higher in PC than in BPH. According to the expression of ASK‐1 and Raf‐1, two main profiles were identified: (TRAF‐6+, ASK‐1+, Raf‐1+) and (TRAF‐6+, ASK‐1+, RAF‐1−) in both BPH and PC. In addition, ASK‐1/p38 axis expression was increased in BPH. Raf‐1/ERK signaling pathway was increased in PC samples. On the other hand, representing of individual signaling protein expression enclosing each of p38 and ERK MAP Kinases according to TRAF‐6+ showed a qualitative behavior of ASK61/p38 and Raf‐1/ERK signaling pathways and a dynamic expression of PSA associated with immune and inflammatory process. These findings suggest that prostate epithelial cell could able an immune and inflammatory setting.

In spite of preventive measures such as Papanicolaou cervical cytological analysis and, more recently, vaccination against HPV infection, cancer of the uterine cervix continues to be one of the most frequent causes of mortality among women worldwide, particularly in developing countries. In this prospective study, sixty patients with inflammatory Pap smears had a colposcopy with directed biopsies. The average age of our patients was 42 years. Results showed that colposcopy is normal in 10% of women. It showed normal transformations, ectropion, a colpotis and polyp at 8.33%, 21.66%, 13.33% and 5% respectively. It was able to detect changes with Grade I atypical transformations (28.33%), and Grade II atypical transformations in 13.33% of cases. The biopsies were objectified dysplasia and carcinoma in 24.13% of cases with carcinoma in situ, micro invasive squamous cell carcinoma and invasive carcinoma glandular. Moreover, we detected HPV-specific antibodies in sera of these patients. Results showed that six patients (10%) showed a positive reactivity to at least one of the HPV-16 or HPV-18 antigens and sera showed different reactivity to the different antigens with the following percentages: 5%, 3%, 2%, 3% and 3% for L1 HPV-16, E6 HPV-16, E7 HPV-16, E6 HPV-18 and E7 HPV-18 respectively. Among patients having positive antibody response, 83.33% were cases of dysplasia and carcinoma. We concluded that the Pap smear, examination of key screening for cervical cancer, is a screening test without diagnostic value and more specifically any inflammatory Pap smear should be considered a positive test and led to further investigations. Moreover, colposcopy is an exam that is performed on an outpatient basis; it allows a detailed study of the cervix and reduces the negative rate of cytology. In addition, early detection of HPV antibodies could help the follow-up of patients.

Antibody detection depends on the type of antigen, and is well correlated with international scientific findings. The differences in antibody response between patients with inflammation and patients with cervical cancer were significant.