Ardekani Omid Salahi, Letafati Arash, Dehkordi Sepehr Ebrahimi, Farahani Ali Vasheghani, Bahari Mahshid, Mahdavi Bahar, Ariamand Negar, Taghvaei Mahdie, Kohkalani Moein, Pirkooh Angila Ataei, Jazayeri Seyed Mohammad, Saso Luciano
Research Center for Clinical Virology, Tehran University of Medical Science, Tehran, Iran.
Department of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.
Eur J Med Res. 2025 Apr 28;30(1):339. doi: 10.1186/s40001-025-02605-4.
Infertility has emerged as a significant global health concern, affecting nearby 8-12% of couples in reproductive age worldwide. Increasing evidence suggests a potential link between human papillomavirus (HPV) and infertility in both men and women. Some research indicate that HPV can infect various components of semen, potentially affecting sperm quality by decreasing motility, viability, and increasing DNA fragmentation, all of which may contribute to male infertility. The virus can attach to the equatorial region of the sperm head, enabling infected sperm to transmit the virus to the oocyte or placenta. Consequently, HPV potentially induces apoptosis in trophoblastic cells and disrupts their adhesion to endometrial cells, which raises the risk of miscarriage. HPV may also affect ovarian reserve by causing chronic inflammation, which can impair granulosa cell function and lower serum anti-Müllerian hormone (AMH) levels. Besides, HPV-related immune responses also contribute to infertility by producing anti-sperm antibodies (ASAs), which cause sperm clumping, reduce motility through cervical mucus, activate the complement system that damages sperm in the female reproductive tract and interfere with sperm-egg interactions. Moreover, HPV infection has been linked to reduced success rates in assisted reproductive technologies (ART), potentially disrupting critical processes such as the acrosome reaction, sperm-oocyte interaction, and fusion. One potential mechanism through which HPV contributes to infertility is oxidative stress (OS). Triggered OS can negatively impact sperm quality and cause damage to the female reproductive system, ultimately contributing to infertility. Despite these associations, the precise mechanisms and the strength of the relationship remain uncertain. Thus, this review seeks to investigate the potential impact of HPV on infertility, particularly its effects on the reproductive system through OS. A clearer understanding of these processes could inform future health strategies for addressing HPV-related infertility.
不孕症已成为一个重大的全球健康问题，影响着全球近8%-12%的育龄夫妇。越来越多的证据表明，人乳头瘤病毒（HPV）与男性和女性的不孕症之间存在潜在联系。一些研究表明，HPV可感染精液的各个成分，可能通过降低活力、存活率和增加DNA碎片化来影响精子质量，所有这些都可能导致男性不育。该病毒可附着于精子头部的赤道区域，使受感染的精子将病毒传播至卵母细胞或胎盘。因此，HPV可能诱导滋养层细胞凋亡并破坏其与子宫内膜细胞的黏附，从而增加流产风险。HPV还可能通过引起慢性炎症影响卵巢储备，这会损害颗粒细胞功能并降低血清抗苗勒管激素（AMH）水平。此外，HPV相关的免疫反应也通过产生抗精子抗体（ASA）导致不孕，抗精子抗体可导致精子凝集，降低精子通过宫颈黏液的活力，激活补体系统，损害女性生殖道中的精子，并干扰精卵相互作用。此外，HPV感染与辅助生殖技术（ART）成功率降低有关，可能会破坏顶体反应、精卵相互作用和融合等关键过程。HPV导致不孕的一种潜在机制是氧化应激（OS）。引发的氧化应激会对精子质量产生负面影响，并对女性生殖系统造成损害，最终导致不孕。尽管存在这些关联，但确切机制和关系强度仍不确定。因此，本综述旨在研究HPV对不孕症的潜在影响，特别是其通过氧化应激对生殖系统的影响。对这些过程的更清晰理解可为未来应对HPV相关不孕症的健康策略提供参考。
