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Cervical cancer is the third most common cause of cancer-related death in women worldwide. Infection with high-risk human papillomavirus (HPV) is established as the cause of cervical carcinoma, therefore, high risk HPV detection may have prognostic significance for the women who are at increased risk of disease progression. The paucity of data on the incidence of cervical cancer in Pakistan makes it difficult to determine disease burden. Even less information is available regarding the prevalent HPV strains in cervical specimens collected from this region. Cervical cancer is a neglected disease in Pakistan in terms of screening, prevention, and vaccination. Identification and accurate genotyping of the virus burden in cancer specimens is important to inform intervention policies for future management of HPV associated disease and to potentially stratify patients dependent on HPV status. In this study, detection and genotyping of HPV types 16 and 18 from 77 cervical specimens were carried out. Consensus primers GP5+/GP6+, which detect 44 genital HPV types, and type specific primers (TS16 and TS18) were used in conjunction with newly designed type specific primers. Using a combination of these methods of detection, a total of 94.81% (95% CI ±4.95) of cervical lesions were positive for HPV. Single infections of HPV16 were detected in 24.68% (95% CI ±9.63) of total samples and HPV18 was found in 25.97% (95% CI ±9.79) samples. Interestingly, a high proportion of samples (40.26%, 95% CI ±10.95) was positive for both HPV16 and 18, indicating a higher incidence of co-infection than previously reported for similar ethnic regions. The HPV genotype of 3.90% of HPV positive samples remained undetected, although these samples were positive with the GP5+/GP6+ primer set indicating infection with an HPV type other than 16 or 18. These data indicate that the overall incidence of high risk HPV infection in cervical cancer and intraepithelial neoplasia specimens in Punjab, Pakistan is in line with the worldwide prevalence, but that the incidence of HPV16 and 18 co-infections in our cohort is higher than that previously reported.

Objective: Cervical carcinoma is one of the most common diseases in our setup studies show that it is preceded by precursor lesions. It has been suggested that persistent infections with human papillomavirus (HPV) is the major risk factor in the development of this invasive cervical neoplasia. The rationale of this study was, whether detection may contribute to the identification as a major risk factor in cervical neoplastic lesions. Study Design: Experimental study. Methods: 102 cases were selected after screening 1000 specimens through Papanicolaou stains of cervical cytology and histopathology for detection of HPV and its subtype PCR. Data for risk factors were collected by a questionnaire and association of HPV was seen with Positive PCR results. Patient demographics including their age, sexual partners, marital status, socioeconomic condition, contraceptive and screening history were evaluated to determine whether subsidiary risk factors are associated with HPV and the development of cervical lesions among Pakistani women. Major Outcome: 85% cases of cervical carcinoma were associated with high risk HPV infection. Results: 46/102 (45%) cases were low grade squamous cell intraepithelial lesions(L-SILs),twenty two (21.5%) cases were high grade squamous cell intraepithelial lesions (H-SILs), 14(13.7%) cases were squamous cell carcinomas(SCC), 6 (5.8%) cases showed features of adenocarcinoma, 10(9.8%) cases showed cytology of atypical squamous cells of undetermined significance(ASCUS) and 4(3.9%) cases were of atypical glandular cells of undetermined significance(AGUS). Out of 102 cases, 88/102(86.27%) were positive for HPV and among them 32/88 (36%) cases were of HPV-16 and 56/88(64%) cases of HPV-18. There was strong association of HPV positivity with young age, early marriages, poor socioeconomic condition, abortions, multiparity and smoking but there was no association with multiple marriages. Conclusion: Frequency of HPV-18 was greater than HPV-16 in cervical neoplastic lesions and was strongly associated with certain known risk factors for cervical carcinoma.

Background: Since the identification of HPV as the necessary cause of cervical cancer, knowledge of its natural history for cervical infection; genotypes, load and form, is essential to prevent and predict cervical carcinoma. A cross sectional study was conducted to see the natural history and genotypes of HPV in cervical neoplastic lesions. Materials and Methods: Two diagnostic modalities, IHC and PCR, were performed on 102 diagnosed cases of cervical premalignant and malignant lesions (Cervical Neoplastic Lesions: CNL) and lesions by histopathology. Results: Out of the102 cases there were 12, 44,40 and 6 cases of Squamous cell Papilloma(SCP), Squamous Cell Dysplasia(CD), Squamous Cell Carcinoma(SCC) and Adenocarcinoma(ADC) respectively. There were 82 CNL, which showed positive HPV reaction on IHC while 88 CNL showed presence of HPV (56/88:64% HPV-18 and 32/88:36% HPV-18) on PCR. There was significant association between the presence of HPV and p53 mutation among different CNL. There was no statistical difference in lesions with respect to positivity of HPV and P53 suggesting that the expression of this suppressor gene was affected by the presence of the HPV genome, p-value>0.05.IHC scoring of CNL was not significantly affected with HPV infection (p-value>0.05). The overall sensitivity, Specificity and accuracy of IHC against PCR was 93%,70,89% merits and demerits of each modality has also been given in detailed. The major mode of infection of HPV-16 was host nuclear integration (p:0.000) with different variant with predominant E-350G genotype(p:0.000). High Viral load was seen in infected cervical tissues. Conclusion: HPV-18&16 were detected;E-350 G genotype was most common form while predominant way of infection was host nuclear integration of HPV. The etiological involvement of HPV in the development of CNL was found because of high viral load and significant association with p53 protein expression with HPV infection. Citation Information: Cancer Prev Res 2011;4(10 Suppl):A115.