Detection of CD155 Marker in Benign Prostate Hyperplasia Patients Infected with Human Papillomavirus

Document Type : New and original researches in the field of Microbiology.

Authors

1 Department of Microbiology, College of Medicine, University of Anbar

2 Department of Surgery, College of Medicine, University of Anbar

Abstract

Background: Human Papillomavirus (HPV) has been implicated in the pathogenesis of Benign Prostate Hyperplasia (BPH), suggesting a potential viral influence on the disease's development and progression Objctive: This study aims to Detection of CD155 marker in molecular Diagnosed Human papillomavirus patients infected with Benign Prostate Hyperplasia (BPH). Methodology: Prostate tissue samples from 50 BPH patients in Ramadi City were collected between December 2023 and April 2024. After PSA and ultrasound confirmed BPH cases, PCR-based HPV16 and HPV18 genotyping was carried out. Twelve of the 39 samples with positive HPV16 tests also tested positive for HPV18. In the eleven samples that did not test positive for HPV16 or HPV18 by PCR, further analysis was performed to confirm the expression of CD155. Results: In 50 prostate tissue samples, total PSA was higher in patients with enlarged prostates (9.82 ± 4.33 ng/ml) than in those with normal prostates (7.04 ± 4.51 ng/ml), while free PSA was lower (0.35 ± 0.12 ng/ml vs. 0.48 ± 0.23 ng/ml), though differences were not statistically significant (p=0.272, p=0.171). For PCR16-positive patients (n=39), total PSA was slightly higher (11.95 ± 6.39 ng/ml) than in PCR16-negative patients (9.50 ± 4.65 ng/ml), with free PSA levels of 0.38 ± 0.14 ng/ml and 0.31 ± 0.12 ng/ml, respectively (p=0.648, p=0.412). PCR18-positive patients (n=12) had a total PSA of 9.05 ± 5.01 ng/ml, compared to 12.16 ± 7.55 ng/ml in PCR18-negative patients (p=0.550), while free PSA levels were similar (p=0.738).CD155 expression was significantly associated with HPV infection. Among PCR16-positive patients, 92.1% had positive CD155 expression (p<0.001), while all PCR18-positive patients (100%) showed CD155 positivity, compared to only 2.6% of PCR18-negative patients (p<0.001. Conclusion: With a substantial association between HPV16 and CD155 marker expression, our work demonstrates the significant occurrence of HPV16 and HPV18 in BPH patients. According to these results, HPV infection may have a part in modifying CD155 expression, which could aid in the pathophysiology of BPH. The underlying processes and possible diagnostic and therapeutic consequences of this connection require more investigations.

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