Namavar Jahromi B, Yaghobi R, Matlub N, Fazelzadeh A, Ramzi A, Anvar Z, et al . P-122 Prevalence of cytomegalovirus in semen of male partners of infertile couples and the virus impact on sperm parameters. IJRM 2021; 19 (5) :289-289
URL:
http://ijrm.ir/article-1-3033-en.html
1- Infertility Research Center, Shiraz University of Medical Sciences, Shiraz, Iran. , namavarb@sums.ac.ir
2- Shiraz Transplant Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
3- IVF Section, Ghadir Mother and Child Hospital of Shiraz, Shiraz, Iran.
4- Department of Obstetrics and Gynecology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.
5- Infertility Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
6- Department of Pediatrics, Shiraz University of Medical Siences, Shiraz, Iran.
7- Molecular Medicine Department, School of Advanced Medical Sciences and Technologies, Shiraz University of Medical Sciences, Shiraz, Iran.
Abstract: (441 Views)
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.
Objective: 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.
Materials and Methods: In this cross sectional study, CMV DNA and virus copy number were ex-amined 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 p-values 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 ab-normal 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 pa-rameter 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 pres-ence of CMV, are in favor of the negative impact of CMV on male fertility.
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