Introduction
Human papillomavirus (HPV) is the most common sexually transmitted infection worldwide and causes substantial morbidity in both sexes. HPV is the main etiologic agent of the cervix, vagina, vulva, penis, oral cavity, head and neck, and anal canal cancers. Oncogenic types, also called high-risk types (HR HPV), can cause penile squamous cell carcinoma. Infection with non-oncogenic types, associated with low oncological risk, causes mainly oligosymptomatic, spontaneously transient infections of the genitourinary organs of both women and men. Of these, types 6 and 11 are most often responsible for the occurrence of genital warts in males. Although men are regarded as a dominant factor in infection transmission to their female sexual partners, they usually do not develop clinically significant HPV-related lesions, and infections are relatively short-lasting [1].
Few epidemiological studies have been conducted in Europe on the presence of HPV in the male population. There is a relatively large amount of data on the American population (mainly from California, Brazil, and Mexico) and Asian population; however, it differs significantly from the European population regarding racial, genetic, cultural, and social structure [2–6].
Meta-analysis of 31 articles about the prevalence of genital HPV DNA among men in northern, southern, and western Europe revealed that the HPV prevalence in the general population was 28.5% and in men in the high-risk population was 30.9%. HPV-16 was the most prevalent high-risk type in both populations [7].
There is little data from Eastern Europe. The latest Report of ©ICO/IARC Information Centre on HPV and Cancer, dated 2023, contains no information about the HPV prevalence in men in Poland [8].
The p16 tumour suppressor protein, an important cell cycle regulator, is encoded by the INK4A gene localized in chromosomal region 9p12 [9]. It stops cell division in the G1 phase, preventing it from proliferating [10]. Mature epithelial cells have barely detectable levels of p16 protein. On the other hand, cells infected with the oncogenic HPV virus exhibit a significantly increased level of expression of this protein, resulting from the neutralization of anti-oncogenes p53 and pRB by viral oncoproteins E6 and E7 [11]. Increased expression of p16INK4a has been shown to correlate with a higher degree of cellular dysplasia and an increased risk of cancer progression [12]. Therefore, in recent years, p16 has become a widely used marker of high-risk HPV infection [13, 14].
Aim
Our aim in this study was to define the prevalence of the most common types of HPV associated with high risk of proliferative process of the epithelium (HPV-6, -11, -16, -18, -31, -33, -35, and -45) in penile localization in the population of asymptomatic Polish men, and to assess whether the infections are associated with high probability of penile squamous cell carcinoma, based on the presence of protein p16INK4a.
Material and methods
Study population
DNA testing for HPV viruses and the expression of the p16INK4a protein were analysed in the material purified from three penile sites (urethral meatus, coronal sulcus, and inner foreskin) in 100 Polish men, aged 20 to 80, who were consecutively admitted to the Department of Forensic Medicine at the Medical University of Warsaw due to sudden death. The study is retrospective and observational in nature. The study was approved by the Bioethics Committee of the Medical University of Warsaw, and the procedures used comply with the Declaration of Helsinki and the Polish Act of 1 July 2005, on the Collection, Storage, and Transplantation of Cells, Tissues, and Organs.
The primary inclusion criterion was the absence of macroscopic pathological changes on the penile skin and mucosa. The study excluded men with phimosis, a history of penile surgery (primarily circumcision), visible abnormalities or narrowing of the urethral meatus, macroscopic pathological changes in the foreskin and/or glans, including genital herpes and penile oedema, as well as those with herpes labialis, documented bladder catheterization within a month before death, or documented death due to sepsis. The final study population comprised 52 men.
Conventional immunohistochemistry in light microscopy
Immunohistochemical reactions were performed on 4 µm-thick paraffin-embedded tissue sections using peroxidase activity in an enzymatic reaction. After deparaffinization and rehydration, the samples underwent epitope retrieval. To detect the target protein, the primary antibody Anti-CDKN2A/p16INK4a (2D9A12, catalogue no. ab54210, Abcam, Cambridge, UK) was used. The samples were then incubated in a 3% hydrogen peroxide solution to block endogenous peroxidase activity, followed by treatment with a 5% donkey serum solution to prevent non-specific antibody binding. Next, the samples were incubated with the primary antibody solution, followed by a washing step and incubation with secondary antibodies conjugated with peroxidase (catalogue no. DS9800, Leica Biosystems, Wetzlar, Germany). The reaction was visualized using 3,3’-diaminobenzidine as a chromogen, and cell nuclei were counterstained with hematoxylin.
Immunohistochemical reactivity was assessed using the IRS (Immunoreactive Score) scale [15]. The number of positively stained cells (PC) was evaluated with semiquantitative scores: 0 – no positive cells; 1 – up to 10% of positive cells; 2 – 11–50% of positive cells; 3 – 51–80% of positive cells; 4 – > 80% of positive cells. The reaction intensity (RI) was scored as follows: 0 – no reaction; 1 – weak reaction; 2 – moderate reaction; 3 – strong reaction. Each sample was analysed in at least five fields of view under a light microscope at 20× magnification. The final IRS was calculated as the product of PC and RI, with the final score determined based on the average values from five fields of view. The IRS for p16INK4a ranged from 0 to 12 and was categorized as follows: 0–2 – weak reaction; 3–5 – moderate reaction; 6–12 – strong reaction.
Detection and typing of human papillomaviruses
For HPV detection and typing, DNA was isolated from 20–50 µg of fresh, rapidly frozen tissue fragments collected from three different penile sites using the NucleoSpin Tissue DNA kit (Macherey-Nagel, Dueren/Düren, Germany). The samples were analysed in a two-step manner. First, HPV DNA detection was performed using SYBR-based real-time PCR (qPCR) with the SensiFAST SYBR Kit (Bioline-Meridian, London, UK) and GP5+/6+ primers, which are complementary to conserved regions of the L1 gene, with the confirmation of the product specificity via melting curve analysis [16]. Next, to confirm the presence of HPV DNA in positive samples and to determine the HPV type, an additional qPCR assay was conducted using primers and dual-labelled probes specific for HPV-6/11, -16, -18, -31, -33, -35, and -45. A detailed description of the method has been published previously [17]. Additionally, all samples were analysed with a set of primers and a probe specific for human glucose-6-phosphate dehydrogenase (G6PD) to confirm DNA isolation from tissue and, for positive samples, to normalize the viral DNA copy number per number of cellular DNA copies. The virus-specific and cellular gene-specific qPCR reactions were performed using the SensiFAST Probe No-ROX Kit (Bioline-Meridian, London, UK). All qPCR reactions were conducted on a CFX96 Real-Time PCR Detection System (BIO-RAD, Marnes-la-Coquette, France).
Results
HPV DNA was detected in 7 out of 52 individuals (13.5%). The most prevalent virus type was HPV-18 (3 individuals), while other HPV types were found in single cases (HPV-16, -33, and -45). In 1 case, a co-infection with HPV-6/11 and HPV-16 was identified.
HPV DNA was present in all tested samples (urethral meatus, coronal sulcus, and inner foreskin) in 4 individuals (two infections with HPV-18, 1 with HPV-16, and one co-infection). In 3 cases, HPV DNA was detected in only a single sample (HPV-18 in the inner foreskin, HPV-33 and -45 in the urethral meatus). The number of HPV DNA copies detected in the samples was normalized to 1000 copies of cellular DNA, ranging from 1 to 2580 copies (mean: 270 copies; median: 30 copies).
The median IRS for p16INK4a in the examined tissue samples was 2.6 (range: 0–10.5), indicating a weak reaction on the 0–12 IRS scale. IRS values corresponding to a weak reaction (0–2) were found in 34 individuals (65.4%); moderate reaction (IRS 3–5) in 17 individuals (32.7%); and strong reaction (IRS 6–12) in only one individual. In the group where HPV DNA was detected, the median p16INK4a IRS was 3.0 (range: 1.2–10.5), whereas in the group without HPV infection, the median was 2.6 (range: 0–5.2); p = 0.18.
IRS results did not differ significantly between samples collected from different penile sites in the same individual; the average difference in IRS measurements was 0.45. There was no significant association between the presence or viral load of HPV and the level of p16INK4a expression (correlation coefficient = 0.27; p = 0.33). The median IRS in samples containing HPV DNA was 3.0, while in HPV-negative samples, it was 2.6. Similarly, no statistically significant association was found between the level of p16INK4a expression and the presence or number of HPV DNA copies when the analysis was conducted separately for each of the three examined locations.
A strong reaction was observed in only one individual (sample no. 52), co-infected with HPV-6/11 and HPV-16, with more abundant HPV-6/11 and low-copy HPV-16. Conversely, a weak p16INK4a expression was observed in the sample from the individual with the highest HPV DNA copy number (sample no. 35, HPV-18).
The results are summarized in Tables 1 and 2.
Table 1
Comparison of p16INK4a expression in 52 asymptomatic males, regarding the presence of HPV DNA in tissue
| Variable | Final immunofluorescence score in tissue sampled from: | ||
|---|---|---|---|
| Urethral meatus | Coronal sulcus | Inner foreskin | |
| HPV DNA detected (N = 7) | 2.2* (1.2–3.6)** | 2.6 (1.4–3.4) | 2.8 (2.2–5.2) |
| HPV DNA not detected (N = 45) | 2.6 (1.7–3.3) | 2.8 (1.7–3.6) | 2.2 (1.7–3.0) |
Table 2. Comparison of DNA HPV detection and p16INK4a expression
| Sample no. | Localization | HPV type detected (type, number of DNA copies per 1000 cells) | Number of HPV DNA copies per 1000 cells | Final immunofluorescence score for p16INK4a |
|---|---|---|---|---|
| 1. | Urethral meatus | HPV-18 | 3 | 1.2 |
| Coronal sulcus | 4 | 3 | ||
| Inner foreskin | 4 | 2.8 | ||
| 11. | Urethral meatus | HPV-33 | 73 | 3.6 |
| Coronal sulcus | Not detected | – | 3.4 | |
| Inner foreskin | – | 3.4 | ||
| 20. | Urethral meatus | HPV-16 | 9 | 1.8 |
| Coronal sulcus | 30 | 1.4 | ||
| Inner foreskin | 43 | 2.2 | ||
| 30. | Urethral meatus | HPV-45 | 1 | 1.2 |
| Coronal sulcus | Not detected | – | 1.4 | |
| Inner foreskin | – | 1.6 | ||
| 35. | Urethral meatus | HPV-18 | 941 | 2.2 |
| Coronal sulcus | 2580 | 2.6 | ||
| Inner foreskin | 19 | 2.2 | ||
| 43. | Urethral meatus | Not detected | - | 2.6 |
| Coronal sulcus | - | 2.6 | ||
| Inner foreskin | HPV-18 | 2 | 5.2 | |
| 52. | Urethral meatus | HPV-6/11 + HPV-16 | 84/1* | 9.6 |
| Coronal sulcus | 284/6 | 10.5 | ||
| Inner foreskin | 84/1 | 8.4 |
Discussion
Asymptomatic HPV infections in men represent a significant diagnostic and epidemiological challenge. In contrast to the female population no analogous screening approach for sexually transmitted HPV infections has been adopted in men. The only exception is the French guidelines recommending screening in men having sex with men (MSM) living with HIV [18].
This study analysed the presence of HPV DNA in the penile region of individuals with no clinical symptoms indicative of HPV infection. The epidemiological scale of asymptomatic penile HPV infections remains poorly understood, and published data from various countries report divergent results [19–31] (Table 3). Depending on the characteristics of the studied group and the detection methods used, the proportion of positive samples ranges from 1.3% to 44.6% in adult populations [28, 29] and from 0% to 83.8% in children [20, 30].
Table 3. The results published to date on the presence of HPV DNA in the penile region in the absence of symptoms
| Reference | Country | N | Age | % of positive samples | Sample | Method of HPV DNA detection | Genotypes detected |
|---|---|---|---|---|---|---|---|
| [23] | Germany | 530 | 16–79 | 5.8 | Swabs | Dot-blot hybridization | HPV-6/11 HPV-16/18 |
| [25] | Finland | 432 | 18 | 7.1 | Swabs | PCR | ND |
| [29] | Japan | 74 | 18–35 | 1.3 | Swabs | Hybrid capture | High-intermediate risk |
| [26] | Denmark | 374 | 19–22 | 33.8 | Swabs | PCR + ELHA* | Mostly low-risk (LR) |
| [28] | Mexico | 1030 | 16–40 | 44.6 | Swabs | Blot hybridization of PCR products | Mostly high-risk (HR) |
| [27] | Austria | 250 | 0–10 11–20 > 20 | 50 15.2 34.8 | Tissue (prepuces) | In-situ hybridization | HR: 49.8% LR: 41.9% |
| [30] | Turkey | 30 | 4–11 | 83.8 | Tissue (prepuces) | qPCR | HPV-16 and HPV-18: 3.8% Other: 80% |
| [21] | Croatia | 330 | 17–60 | 32 | Swabs | Roche AMPLICOR HPV | HR: 36% HPV-6: 24.2% HPV-16: 17.8% HPV-51: 8.8% Other: 5% |
| [24] | Austria | 226 | 0–89 0–10 11–20 21–89 | 9.3 4.5 2.1 2.6 | Tissue (prepuces) | qPCR | HR: 4% LR: 5.3% |
| [31] | Poland | 826 | 19–80 | 26.8 | Tissue | qPCR | ND |
| 44.3 | Swabs | Hybrid Capture 2 | LR: 30% HR: 14.3% | ||||
| [19] | Brazil | 110 asymptomatic | 18–67 | 16.4 | Swabs | PCR | HR: 1% |
| 30 phimosis | 18–56 | 43.3 | Tissue | HR: 53.8% | |||
| [20] | Turkey | 62 | 3–11 | 0 | Tissue (prepuces) | SYBR-green-based qPCR | ND |
| [22] | Iran | 415 | 18–30 31–40 41–50 > 50 | 4.0 12.2 2.6 0.9 | Swabs | qPCR | HPV-16: 25.3% 3.6% - HPV-18: 3.6% other HR: 54.2% co-infections: 16.9% |
| This study | Poland | 52 | 20–80 | 13.5 | Tissue | qPCR | Table 2 |
The results of the only study to date assessing the prevalence of HPV in the population of asymptomatic Polish men were published in 2013 [31]. In this multicentre study, two types of material were collected: swabs and tissue samples, although the specific anatomical site on the penis from which they were obtained was not indicated. Two different methods were used to detect viral DNA: Hybrid Capture 2 for swab samples and qualitative real-time PCR for tissue samples, yielding detection rates of 44.3% and 26.8%, respectively. In the present study, HPV infection was identified in 13.5% of men, which is almost exactly half the rate reported by Walczak et al. who examined a much larger group of men – this may partially explain the discrepancy [31]. Another reason may be the difference in subject selection: in Walczak et al.' study, the participants were individuals attending STI clinics, and some of them presented with lesions in the penile area suggestive of HPV infection, while others reported infection in their partners whereas in our study, the group selection can be considered random. These factors may have contributed to an overestimation of HPV DNA detection. Difficulties in comparing the results of analogous studies are not limited to Poland.
The methodology used to detect HPV DNA varies throughout the studies published so far, both in terms of the tested material (swabs from various penile locations, urine, or foreskin fragments obtained from circumcised patients) and the techniques of detection (conventional PCR, qPCR, in situ hybridization, or PCR-hybridization). In the present study, superficial tissue specimens were collected from three different penile locations (urethral meatus, coronal sulcus, and inner foreskin) – regions considered likely sites of HPV transmission during sexual contact. To the best of our knowledge, such an approach has not been used in previous studies. Only in the study by Flores et al. [32], which analysed swabs from multiple genital sites, was it confirmed that HPV detection rates depend on the sampling location – with the highest rates observed in the glans and foreskin areas – findings consistent with the results of the present work. Previous attempts to use urine as a material for assessing HPV infection have yielded unsatisfactory results due to low sensitivity [33].
Further differences arise from the molecular techniques applied. PCR protocols using MY09/MY11 or GP5+/GP6+ primers may vary in terms of sensitivity and the range of detectable HPV genotypes [34–36]. Heidegger et al. [24] attempted a comparison between the sensitivity of in situ hybridization (ISH) and qPCR, showing that ISH may yield inflated positive results, whereas qPCR offers greater specificity, albeit at the cost of lower sensitivity. That study also highlighted the risk of reduced sensitivity when using formalin-fixed paraffin-embedded tissues rather than freshly collected or frozen samples. A meta-analysis by Lee et al. [37] emphasized that the heterogeneity of the results of HPV detection among children and adolescents is partly attributable to methodological differences, both in DNA isolation protocols and in result interpretation. The risk of false-positive qPCR results when using the non-specific SYBR Green dye was analysed by Agras et al. [20], who recommended performing melting curve analysis for all positive samples in the presence of a control containing HPV DNA.
Previous studies on HPV DNA in asymptomatic men have relied on qualitative analyses. In the present study, a quantitative approach was employed, providing an estimate of the number of virus-infected cells or the level of viral DNA replication (without distinguishing between the two), though it does not directly indicate the number of infectious virions. However, considering that the tissue samples were collected from superficial sites where virion production is likely during infection, the HPV DNA copy number is expected to correlate with the potential of virus transmission.
Among the studied group, most cases revealed low levels of HPV DNA. However, in 2 cases (no. 35 and no. 52), the viral DNA index indicated a high number of HPV copies despite the absence of macroscopically visible symptoms. This suggests that at least two out of the 100 participants could be considered potential asymptomatic sources of HPV transmission.
The second parameter assessed in the study was the expression of p16INK4a protein, a widely used cellular marker in the assessment of high-risk HPV infections, especially in women in the context of cervical cancer screening [38, 39]. The role of this marker in HPV-associated precancerous lesions in men is becoming increasingly documented, although its diagnostic significance remains ambiguous [40, 41]. In this study, we addressed a key question: whether asymptomatic HPV infections are associated with elevated p16INK4a expression. The results indicate that, statistically, p16INK4a expression levels in asymptomatic individuals are low and do not differ significantly between HPV-positive and HPV-negative groups. The single sample set no. 52 stands out in which co-infection with HPV-6/11 and HPV-18 was detected, with a high HPV-6/11 DNA copy number and markedly elevated p16INK4a expression accompanying the infection.
The body of literature addressing elevated p16INK4a expression associated with HPV infection in patients without overt clinical signs is limited: it is sometimes observed in HPV-associated precancerous lesions such as anal intraepithelial neoplasia (AIN) and penile intraepithelial neoplasia, where the intensity of expression correlates with viral presence and the tissue’s oncogenic transformation potential [42]. In HIV-positive men, significantly increased p16INK4a expression can be present in low-grade AIN, suggesting subclinical HPV infection with oncogenic potential [43]. The case we identified – an asymptomatic infection with high HPV DNA copy number and elevated p16INK4a expression – suggests, on the one hand, the potential for effective transmission of infection, and on the other, highlights the value of screening for early identification of individuals in whom HPV may pose an oncogenic risk.
In the context of asymptomatic or paucisymptomatic HPV infections, the potential utility of biomarkers other than p16INK4a for identifying precancerous conditions or assessing tumour progression can be discussed. In penile cancers, an association between p53 gene mutations and the risk of malignant transformation, prognosis, and survival has been confirmed [44]. From a more practical perspective, a combined diagnostic approach incorporating the assessment of viral oncogene (E6, E7) expression levels together with the evaluation of cellular proteins p16INK4a and p53 has been proposed; however, such studies have not yet been conducted in the context of penile cancer. Moreover, no standardized methodology exists for the immunohistochemical evaluation of p53 expression [45]. Additional investigations have explored the potential relevance of assessing the expression of Ki67, PIK3CA, APOBECs, caveolin-1, and nectin-4, though no definitive conclusions have been reached regarding their practical value in estimating the risk of HPV-related penile cancer [44, 46–50].
18F-fluorodeoxyglucose–positron emisson tomography/computed tomography (18F-FDG PET/CT) is a diagnostic modality useful for tumour detection and staging, treatment planning, and monitoring therapeutic response [51]. This technique has also been applied in the evaluation of neoplastic lesions located in the penile region [52], although its greatest utility is observed in cases of T1 or higher stages and in the presence of local or distant lymph node metastases, whereas its sensitivity in cN0 patient groups remains unsatisfactory. Furthermore, diagnostic performance varies considerably depending on the centre performing the examination [53]. Recently, Salazar et al. demonstrated that 18F-FDG PET/CT is not useful for differentiating HPV-related penile tumours from those of other aetiologies [54]. Interpretation of 18F-FDG PET/CT findings is further complicated in the presence of inflammation or infection, as the tracer uptake pattern in inflammatory foci is virtually indistinguishable from that of malignant lesions [55, 56].
The practical significance of asymptomatic HPV infections in men remains a topic of debate, yet several important factors deserve attention. First, asymptomatic carriers may serve as sources of infection for their sexual partners – this concerns primarily infections localized to the genital region, but also includes the anal and oral areas. Research by Nyitray et al. [57] demonstrated that even asymptomatic men can transmit HPV to their partners, particularly when the virus is present at multiple penile sites. A study by Benevolo et al. [58] conducted among men whose female partners were infected with HPV often found concordance in viral genotypes, supporting the significant role of men as reservoirs and sources of infection, even in the absence of symptoms.
Another key aspect of asymptomatic HPV infections is their co-occurrence with other sexually transmitted infections (STIs). As early as 1987, Grussendorf-Conen et al. [23] suggested that the presence of HPV DNA in healthy men might serve as a marker for increased risk of other infections, even if these are not simultaneously present. Later, Takahashi et al. [29] reported that in young, healthy Japanese men, HPV infection frequently coincided with other STIs, including Chlamydia trachomatis, Neisseria gonorrhoeae, and herpes simplex virus. Philibert et al. [59], who analysed samples from MSM, also revealed frequent co-occurrence of HPV with chlamydial and gonorrhoeal infection. This association may stem from similar modes of transmission and epithelial damage, which facilitates secondary infections. Additionally, a global meta-analysis conducted by Bruni et al. in 2023 [60] confirmed that in countries with high STI prevalence, HPV infections in men are frequently associated with other pathogens, particularly among young, sexually active individuals and MSM populations.
A third important aspect of the role of asymptomatic HPV infections in men is the relationship between HPV infection and semen quality and male infertility, even in asymptomatic cases. The underlying mechanisms are complex and include direct effects of the virus on cells, induction of oxidative stress, inflammatory responses, and disruption of sperm DNA integrity [61–64].
A number of risk factors associated with a higher prevalence of penile HPV infection have also been identified. The most important include phimosis, balanitis, obesity, and lichen sclerosus [65–67]. The available literature also indicates an association between poor socioeconomic conditions, cigarette smoking, and psoralen UV-A phototherapy with an increased risk of developing precancerous lesions and progressing to cancer [68–70]. Emphasis is also placed on the role of circumcision as an effective procedure for preventing both HPV infection and the development of virus-related neoplastic lesions [71]. Interesting findings related to the problem of early detection of neoplastic lesions were presented by Skeppner et al. [72]. In the study group, a significant delay in the correct diagnosis of penile carcinoma, lasting 6 months or more, resulted from the nonspecific nature of the lesion – perceived as erythema, rash, or eczema – non-diagnostic histopathological findings, as well as psychological factors delaying the seeking of medical attention. A valuable review of the above issues was provided by Douglawi and Masterson [50].
One of the most important components of effective HPV infection prevention is vaccination. Vaccines show the highest efficacy, the strongest immunogenicity and long-lasting protection when administered during early adolescence (ages 9–14), before the onset of sexual activity [73, 74]. According to WHO guidelines, the primary goal of HPV vaccination programs is to achieve the highest possible coverage among 15-year-old girls [75]. Vaccination in other groups, including boys, is considered a secondary objective by WHO, dependent on local financial and organisational capabilities [75].
Estimates for Europe indicate that approximately 19% of HPV-related cancers occur in men, with the highest proportions in penile cancer and cancers of the head and neck [76]. Most of these cancers are potentially preventable through vaccination, providing a strong argument for including boys in population-wide vaccination programs. The European Union, in its most recent recommendations, advocates vaccinating both girls and boys [77, 78]. However, the success of national vaccination programs depends on numerous factors, not only financial and organisational capabilities but also psychosocial factors, which play a significant role in the decision to vaccinate, especially among boys [79, 80].
Poland, with a visibly growing group of vaccine sceptics, presents a notable example in this regard. The Polish publicly funded HPV vaccination program has a relatively long history: the first nationwide vaccination campaigns, organised at the local level, began in 2010. In 2023, a government-run universal program was launched to vaccinate girls and boys aged 12–13, and in 2024, the age range was extended to those aged 9–14 for the 9-valent vaccine and to 9–18 for the bivalent vaccine [81]. Vaccines are fully reimbursed and may be prescribed by general practitioners.
The program achieved its highest effectiveness in 2010 and 2011, with 26.1% and 30% of eligible children vaccinated, respectively. Since then, vaccination rates have declined, reaching 10.5% in 2023 and 8.6% in 2024. In the same year, the cumulative vaccination rate reached 14%, placing Poland among the countries with the lowest HPV vaccination coverage in publicly accessible programs [82, 83]. A gender disparity is also evident: the cumulative vaccination rate was 17.7% for girls and 10.6% for boys. Vaccination campaigns are more effective in large urban centres: the average cumulative coverage across the five largest metropolitan areas was 23.5%, compared to the average value of 5–10% in rural areas in eastern Poland [84].
Conclusions
Determining the true prevalence of asymptomatic HPV infections in men requires a standardized methodology. Assessing the value of screening in men – and answering the question of whether such testing should be limited to risk groups or extended to a broader population – can also be based on data from asymptomatic individuals. A major challenge that remains to be addressed is the development of effective strategies to improve vaccination uptake in communities where the topic of HPV infections remains taboo.
