Detection of oncogenic viruses (SV40, BKV, JCV, HCMV, HPV) and p53 codon 72 polymorphism in lung carcinoma

As a part of our continuous search for oncogenic viruses in bronchial cancer, we extended our HPV studies to analyse also SV40, BKV, JCV and HCMV sequences in bronchial cancer and related these data with p53 codon 72 polymorphism. Fresh tumor samples from 78 patients with lung cancer were analysed for SV40, BKV, JCV, HCMV and HPV sequences by PCR. HPV genotypes were determined using reverse blot hybridization and sequencing, and all HPV-positive tumors were tested for the presence of E6/E7 transcripts by RT-PCR. All samples were analysed for p53 codon 72 polymorphism, using PCR-based RFLP method. Of the 78 cases studied, 11 (14.1%) were positive for T-Ag gene of SV40, while BKV and JCV sequences were both amplified in 1 tumor only. Altogether, 10/78 lesions were HPV-positive; six HPV16, one HPV31, two HPV6/53 and one HPV16/18. All HPV DNA-positive samples except one also expressed E6 and E7 transcripts. HCMV was amplified in 18 (23%) cases. RFLP analysis of p53 codon 72 revealed 32 homozygotes for arg/arg allele (50.8%), 26 heterozygotes for arg/pro allele (41.3%), and 5 homozygotes for pro/pro allele (7.9%). P53 codon 72 polymorphism was not significantly different between cases (n = 63) and controls (n = 50) (p = 0.455), among virus positive and negative patients, nor was it related to HPV genotypes (p = 0.384), expression of E6 (p = 0.384) and E7 oncogenes (p = 0.293). Of all possible combinations of virus co-detection, only SV40-HCMV association was statistically significant (OR = 5.500, 95%CI 1.43-21.02; p = 0.015). Taken the known mechanisms of these individual viruses, there is a chance that these viruses could affect cell cycle control and inhibit apoptosis, thus potentially causing genetic instability and promote oncogenesis.