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Infertility is a global health problem affecting about 15% of all couples, of which 50% are due to male infertility. Although the etiology of infertility is known in most infertile men, idiopathic male infertility remains a challenge. Therefore, there is a need for novel diagnostic methods to detect the underlying mechanisms and develop appropriate therapies. Recent studies have focused on the role of non-coding RNAs (ncRNAs) in male infertility. Circular RNAs (CircRNAs), a type of ncRNAs, are found to play a key role in the development of some pathological conditions, including cardiovascular diseases, diabetes, cancers, autoimmune diseases, etc. Several studies have reported the presence of CircRNAs and their target genes in the human reproductive system. In addition, their expression in testicular tissues, sperm cells, and seminal fluid has been identified. Abnormal expression of CircRNAs has been associated with azoospermia and asthenozoospermia in infertile men. The present narrative review provides a brief description of the role of CircRNAs in spermatogenic cells, male infertility, and reproductive cancers. In addition, some CircRNAs have been identified as potential biomarkers for disease detection and treatment. [ABSTRACT FROM AUTHOR]

Background: Genital tract infection is one of the causes of male infertility. Several studies have shown a role for human cytomegalovirus (CMV) in this context. In the present study, the prevalence of CMV in a population of male partners of infertile couples was estimated and the impact of CMV on sperm parameters was determined. Methods: In this cross sectional study, CMV DNA and virus copy number were examined in the semen of 150 participants including 80 with normal semen analysis (SA) and 70 with abnormal SA, by quantitative Real-Time PCR. Sperm parameters were compared between CMV positive and negative groups. Comparisons with pvalues under 0.05 were considered significant. Logistic regression was performed to control the effect of some variables with p<0.25 on sperm parameters. Results: CMV DNA was detected in the semen of 28 (18.6%) individuals. 21 men (30%) with abnormal SA and 7 (8.8%) with normal SA were positive for CMV DNA (p=0.001). The mean virus copy number was 883.1±4662.01 for the men with abnormal SA and 2525.7±12680.9 for those with normal SA (p=0.001). Sperm count was (32.1±23.5) x106 in CMV positive and (44.2±24.1) x106 in CMV negative groups (p=0.022). Normal sperm morphology was 2.73±2.83% and 5.99±5.44% in CMV positive and negative groups, respectively (p<0.001). After controlling some variables, the sperm morphology remains the only statistically significant sperm parameter that was reduced by CMV. Conclusion: The higher CMV prevalence in the semen of males with abnormal SA compared to normal SA and significant reduction of sperm morphology in the presence of CMV, are in favor of the negative impact of CMV on male fertility. [ABSTRACT FROM AUTHOR]