ObjectiveThe most common cancer amongst women is breast cancer. Reports on the role of EBV, BKV, and JCV in the development of breast cancer are controversial. Hence, the aim of this study was to determine the frequency of EBV, BKV, and JCV in malignant breast tumors in comparison with benign ones.ResultsA total of 300 breast biopsy tissues were included, of which 150 were malignant and 150 benign. After deparaffinization, tissues were subjected to DNA extraction. β-globin gene was amplified by PCR to evaluate the quality of extracted DNA. In house PCRs assay was performed to detect EBV, JCV, and BKV genome fragment. The mean age of malignant and benign groups was 45.0 ± 9.4 and 35.2 ± 12.1 years old. Out of 150 malignant samples, 146 were ductal, two lobular and two samples both invasive ductal and lobular carcinoma. In the benign group, 96, 52 and two samples were fibroadenoma, fibrocystic, and adenosis types, respectively. Genomic DNA fragment of EBV, BKV, and JCV was not found in any of the malignant and benign breast tissues.ConclusionAccording to our finding, there is the possibility that EBV, BKV, and JCV are not involved in breast cancer pathogenesis.

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Infection with hepatitis A virus (HAV) in patient with chronic liver disease (CLD; due to hepatitis B or hepatitis C) may cause severe disease and fulminant liver failure. This study aimed to determine the seroprevalence of HAV antibodies in patients infected with HCV or HBV in Iran (Jahrom city). A total of 159 patients with underlying CLD were recruited between September 2012 and February 2013. Serum samples were collected from each patient and tested for anti-HAV using enzyme-linked immunosorbent assay (ELISA). The overall seroprevalence of total anti-HAV was 79·2%. Patients aged 20-30 years had the lowest (28·3%) anti-HAV seropositivity and those aged >50 years had the highest (95%) seropositivity. The overall prevalence of anti-HAV in patients with chronic HCV and HBV infection was 93·7% and 77·1%, respectively. The anti-HAV seropositivity in liver cirrhosis patients was 100% compared to CLD patients. Because of low HAV immunity in younger CLD patients, vaccination against HAV should be considered.

Objective: While the vast majority of the cervical lesions have been attributed to the HPVs, the role of EBV and HSV1/2 as co-factors in the progression of these abnormalities needs more investigation. In this study, we aimed to determine the coexistence of EBV or HSV in cervical lesions infected with high-risk HPVs. Methods: Totally, 102 formaline-fixed cervical lesions with different pathological grades (LSIL, HSIL, and SCC) were enrolled in this study. DNA was extracted, and its integrity was examined by PCR assay. Two conventional PCRs were performed for the detection of EBV and HSV1/2 genomes in the tissue specimens. Besides, an in-house Real-Time PCR, as well as a nested PCR assays following sequencing, was performed to detect HPV genotypes in EBV or HSV positive samples. Results: The mean age of the participants was 42.8±13 years. Out of 102 samples, 32% (n=33) were confirmed to be LSIL, 42.2% (n=43) were HSIL, 22.5% (n=23) were SCC and 2.9% (n=3) were adenocarcinoma. EBV genome was detected in 13(12.7%) samples including 2 of LSIL, 8 of HSIL and 3 of SCC. All EBV positive samples harbored high risk HPV types 16,18 and/or 31 co-infections. However, the HSV genome was not found in any of the samples. Conclusion: Our result revealed that the frequency of EBV infection is higher in HISL than LSIL. Moreover, the amount of HPV load showed an elevated level among co-infected patients, which indicates that EBV might be an enhancing factor of disease progression. In contrast, HSV may not has a role as a co-factor in cervical lesions pathogenesis.