Human Papillomavirus and Male Infertility: What Do We Know?

In recent years, increasing attention has been paid to understanding the causes of infertility, which is being recognized as a growing health problem affecting large numbers of couples worldwide. Male infertility is a contributing factor in approximately 30-40% of cases, and one of its etiological causes is sexually transmitted infections (STIs). Among sexually transmitted pathogens, human papillomavirus (HPV) can contribute in various ways to the failure of spontaneous and assisted reproduction, acting in the different phases of conception, especially in the early ones. In particular, HPV infection can affect sperm DNA integrity, sperm motility, count, viability, and morphology and can induce the production of anti-sperm antibodies (ASAs). In this narrative review, we aimed to provide an overview of existing research on the potential adverse effects of HPV infection on male reproductive health. Furthermore, we analyzed how limiting the spread of the infection, particularly with gender-neutral vaccination, could be a possible therapeutic tool to counteract male and female fertility problems.

Orogenital Human Papillomavirus Infection and Vaccines: A Survey of High- and Low-Risk Genotypes Not Included in Vaccines.

Knowledge of human papillomavirus transmission from the genital tract to the oral mucosa remains unsatisfactory, with poor and often inconsistent literature results. The increase in HPV-associated oral malignancies prompts further analysis of the simultaneous detection of the virus in the two anatomical areas and on the identification of genotypes to be included in future vaccines. Therefore, in this retrospective study, we evaluated orogenital HPV concurrence, hrHPV, lrHPV and type-concordance in 337 samples, as well as the prevalence of the most common genotypes not included in HPV vaccines. Concurrence was found in 12.5% (31/248) of cases, hr-concordance in 61.3% (19/31) and lr-concordance in 12.9% (4/31). Finally, type-concordance was found in 32.3% (10/31) of concurrent infections. Regarding the identification of non-vaccine genotypes, the significantly prevalent genotypes in the anogenital area were HPV66 (12.6%, p < 0.0001), HPV53 (11.1%, p < 0.0001), HPV51 (8.7%, p < 0.0001), HPV42 (8.2%, p < 0.0001) and HPV68 (5.6%, p = 0.0034) in women and HPV66 (14.6%, p = 0.0058), HPV42 (12.2%, p = 0.0428), HPV51 (12.2%, p = 0.0428), HPV53 (12.2%, p = 0.0428), HPV70 (12.2%, p = 0.0428) and HPV73 (12.2%, p = 0.0428) in men. Considering the results of our study, we recommend including the high-risk genotypes HPV51, HPV68, HPV53 and HPV66 in future HPV vaccine formulations.

Human Papillomavirus (HPV) Infection and Its Impact on Male Infertility.

Nowadays, the striking numbers of infertile couples that turn to assisted reproductive technologies (ART) drive the research toward a more comprehensive understanding of the underlying causes. Male factors contribute to the inability to conceive in half of the cases, and it has been suggested that sexually transmitted infections could have a role in the onset of spermatozoa impairments. Since the impact of HPV infection on sperm quality and sperm DNA integrity is debated, we wanted to analyze its impact on conventional seminal parameters and the sperm DNA fragmentation index (DFI). Therefore, 117 semen samples of patients undergoing IVF were evaluated for the following characteristics: HPV DNA detection and sperm DNA fragmentation, concentration, motility, and morphology. The results showed a higher rate of HPV-negative patients (59.8% vs. 40.2%) and no HPV-related effect on DFI, sperm concentration, total sperm number, and total motility. Only progressive motility and morphology were found as significantly influenced by HPV positivity. Moreover, we observed a statistically significant difference in DFI when comparing high-risk HPV (HR-HPV) and low-risk HPV (LR-HPV) genotypes. Our data suggest that the presence of any HPV type, whatever the exact localization of the virions, can impair some sperm parameters, while HR-HPVs specifically affect the integrity of spermatozoa DNA.