Unveiling the burden of human papillomavirus infection and risk factors among Indigenous women in Mizoram, Northeast India.

A total of 1018 women between the ages of 20 and 73 years were screened for HPV where 152 (14.9%) patients were found to be HPV positive in the study. The overall enrollment and outcomes of the study are presented in Fig.  1 . There were significantly more of the study participants (78.78%) from Aizawl District, as shown in Fig.  2 . The mean age of the study participants was 41.01 ± 8.833 years. The sociodemographic and participant characteristics are presented in Table 1 . Most of the participants (93.3%) were married, with 78.5% being housewives and 55% having completed high school. Our analysis indicates that participants employed in public service or government sectors have significantly higher odds of HPV infection, with an odds ratio of 1.898 compared to those in other occupations. Betel nut consumption (83.2%) and tobacco chewing (72.8%) were more prevalent among participants than smoking (54.3%) and alcohol consumption (36.3%). The consumption of betel nuts was highly prevalent and was significant ( p  = 0.038) according to the regression analysis. Fig. 1 Flowchart for the enrolled cases for HPV epidemiology. *Low-risk HPV types 6/11. **High-risk HPV types 16, 18,26, 31, 33, 35, 39, 45, 51, 52, 53, 56, 58, 59, 66, 68–73 and 82 Flowchart for the enrolled cases for HPV epidemiology. *Low-risk HPV types 6/11. **High-risk HPV types 16, 18,26, 31, 33, 35, 39, 45, 51, 52, 53, 56, 58, 59, 66, 68–73 and 82 Fig. 2 Number of HPV-DNA Positivity from the District of Mizoram Number of HPV-DNA Positivity from the District of Mizoram Table 1 Participant characteristics and HPV-DNA associations. ( n =1018) Demographic Variables HPV DNA Odds ratio (95% CI) p value Total N (%) Positive N (%) Negative N (%) LOWER 95% CI UPPER 95% CI Age group (in Years) > 20 14 (1.3) 4 (0.3) 10 (0.9) Reference 21–30 95 (9.3) 18 (1.7) 77 (7.5) 0.505 0.135 1.885 0.309 31–40 413 (40.5) 66 (6.4) 347 (34.0) 0.452 0.113 1.537 0.204 41–50 360(35.3) 54 (5.3) 306 (30.0) 0.405 0.118 1.383 0.149 51–60 118 (11.5) 8(0.7) 110 (10.8) 0.155 0.038 0.632 0.009* < 60 18 (1.7) 2(0.1) 16 (1.5) 0.259 0.038 1.761 0.167 Occupation Housewife 800(78.5) 108(10.6) 692 (67.9) Reference Unskilled worker 6 (0.5) 2 (0.1) 4 (0.3) 3.740 0.582 24.052 0.165 Business/private 45(4.4) 9 (0.8) 36 (3.5) 1.769 0.784 3.991 0.169 Employed in Government or Public Sector 100 (9.8) 22(2.1) 78(7.6) 1.898 1.035 3.480 0.038* Self employed 67(6.5) 11 (1.0) 56 (5.5) 1.348 0.658 2.764 0.415 Educational Qualification Primary or below 12 (2) 2 (0.1) 10 (0.9) Reference Middle 71 (6.9) 19 (1.8) 52 (5.1) 1.458 0.256 8.290 0.671 High 560 (55) 75 (7.3) 485 (47.6) 0.702 0.139 3.537 0.668 Secondary 222 (21.8) 36 (3.5) 186 (18.2) 0.720 0.141 3.679 0.693 Graduation 108 (10.6) 15 (1.4) 93 (9.1) 0.521 0.95 2.853 0.453 Post graduation 45(4.4) 5 (0.4) 40 (3.9) 0.414 0.063 2.698 0.356 Marital Status Unmarried 68 (6.6) 10(0.9) 58(5.6) Reference Married 950 (93.3) 142(13.9) 808(79.3) 0.989 0.474 2.064 0.989 Betel Nut consumption Never 171 (16.7) 19 (1.8) 152 (14.9) Reference Frequent 495 (48.6) 61(5.9) 434 (42.6) 0.615 0.295 1.283 0.195 Moderate 352 (34.5) 72 (7.0) 280 (27.5) 1.847 1.036 3.293 0.038* Smoking Never 465 (45.6) 405 (39.7) 60 (5.8) Reference Frequent 333 (32.7) 287(28.1) 46 (4.5) 1.116 0.455 2.738 0.811 Moderate 220 (21.6) 174 (17.0) 46 (4.5) 1.434 0.887 2.319 0.141 Chewing tobacco Never 276 (27.1) 237(23.2) 39 (3.8) Reference Frequent 582 (57.1) 499(49.0) 83 (8.1) 1.069 0.624 1.832 0.807 Moderate 160 (15.7) 130(12.7) 30 (2.9) 1.159 0.657 2.043 0.610 Alcohol consumption Never 648 (63.6) 94(9.2) 554 (54.4) Reference Frequent 286 (28) 41(4.0) 245 (24.0) 2.182 0.848 5.616 0.703 Moderate 84 (8.2) 17(1.6) 67 (6.5) 1.154 0.552 2.414 0.322 *Statistically significant; Cl  Confidence interval, OR  1 risk factor; OR = 1 no difference in the groups Participant characteristics and HPV-DNA associations. ( n =1018) Age group (in Years) *Statistically significant; Cl  Confidence interval, OR  1 risk factor; OR = 1 no difference in the groups The study revealed that the participants presented with a range of clinical characteristics, signs, and symptoms as shown in Fig.  3 . Cervicitis was the most frequently reported clinical or provisional diagnosis, affecting 26.6% of patients, followed by abnormal uterine bleeding at 12.9%. The most common symptom was vaginal discharge, followed by chronic pelvic pain, which was reported in 14.9% and 13.9% of the patients, respectively, whereas only chronic pelvic pain was significantly associated with HPV infection ( p  = 0.002), as shown in Table 2 . The participants’ ages at first pregnancy were recorded in groups, and approximately 648 had their first pregnancy at the age of 21–30 years. The number of pregnancies was categorized into groups, ranging from none to three or more, with the majority of participants ( n  = 674) reporting three or more pregnancies. Interestingly, this group showed a lower likelihood of HPV infection compared to those with fewer or no pregnancies, as indicated by a statistically significant odds ratio (OR = 0.352, 95% CI: 0.133–0.928; p  = 0.035). Age at first, sexual intercourse was found to be significantly associated with HPV infection. Age group 21–25 years (OR = 0.313; 95% CI: 0.137–0.714; p  = 0.006), 26–30 years (OR = 0.315; 95% CI: 0.123–0.804; p  = 0.016), and 31 years and above (OR = 0.268; 95% CI: 0.080–0.871; p  = 0.029) all showed statistically significant protective associations. While the group aged 16–20 years also demonstrated reduced odds (OR = 0.497), this was not statistically significant ( p  = 0.076). The study assessed the use of various contraceptive methods, including oral contraceptive pills, condoms, and copper-T intrauterine devices. Among these, oral contraceptive use was the most common, reported by 436 participants significantly less likely to be HPV positive compared to non-users, indicating a protective association (OR = 0.604, 95% CI: 0.399–0.915; p  = 0.017). In contrast, the use of condoms and copper-T did not show a statistically significant association with HPV infection in this study. Another method of cervical screening, the Pap smear, reported the following results: a percentage of samples were categorized as negative for intraepithelial lesion or malignancy (NILM), a percentage showed low-grade squamous intraepithelial lesions (with one case testing positive for HPV), and a percentage were identified as high-grade squamous intraepithelial lesions, with two cases testing positive. Chi-square analysis revealed these findings to be statistically significant ( p  = 0.025). Fig. 3 Distribution of the percentages of patients with different clinical characteristics of HPV in the study Distribution of the percentages of patients with different clinical characteristics of HPV in the study Table 2 Clinical features and reproductive characteristics. ( n =1018) Description HPV DNA Odds ratio (95% CI) P value Total N (%) Negative N (%) Positive N (%) LOWER 95% CI UPPER 95% CI Post Menopausal Bleeding Yes 8 (0.7) 8 (0.7) 0 (0) No 1010 (99.2) 858 (84.2) 152 (14.9) Vaginal Discharge Yes 152 (14.9) 97 (9.5) 55 (5.4) 1.093 0.732 1.633 0.664 No 866 (85.0) 557 (54.7) 309 (30) Reference Cervicitis Yes 271 (26.6) 240 (23.5) 31 (3.0) 0.841 0.532 1.328 0.457 No 747(73.3) 626 (61.4) 121 (11.8) Reference Cervics Polyps Yes 23 (2.2) 19(1.8) 4 (0.3) 1.465 0.458 4.689 0.520 No 995 (97.7) 847(83.2) 148 (14.5) Reference Borderline Ovarian Tumor Yes 26 (2.5) 23 (2.2) 3(0.2) 1.192 0.337 4.215 0.785 No 992(97.4) 843(82.8) 149 (14.6) Reference Visual Inspection with Acetic Acid Yes 22(2.1) 19(1.8) 3 (0.2) 1.479 0.371 5.897 0.579 No 996(97.8) 847 (83.2) 149 (14.6) Reference Ovarian Cyst Yes 22 (2.1) 22(2.1) 0 (0) No 996 (97.8) 844(82.9) 152(14.9) Adenomyosis Yes 32 (3.1) 30 (2.9) 2 (0.1) 0.525 0.119 2.319 0.395 No 986 (96.8) 836 (82.1) 150 (14.7) Reference Abnormal Uterus bleeding Yes 132 (12.9) 118(11.5) 14 (1.3) 0.841 0.439 1.609 0.600 No 886 (87.0) 748(73.4) 138(13.5) Reference Chronic Pelvic pain Yes 142(13.9) 107(10.5) 35 (3.4) 2.112 1.315 3.392 0.002* No 874 (85.8) 759(74.5) 117 (11.4) Reference Menorrhagia Yes 48 (4.7) 40(3.9) 8 (0.7) 1.381 0.563 3.385 0.480 No 970 (95.2) 826 (81.1) 144 (14.1) Reference Genital Ulcer Yes 9(0.8) 6 (0.5) 3 (0.2) 4.336 0.814 23.107 0.086 No 1009 (99.1) 860(84.4) 149 (14.6) Reference Dyspareunia Yes 22(2.1) 18 (1.7) 4 (0.3) 1.388 0.417 4.623 0.593 No 996(97.8) 848(83.3) 148 (14.5) Reference Poscoital bleeing Yes 14(1.3) 11(1.0) 3 (0.2) 1.815 0.430 7.663 0.417 No 1004(98.6) 855(83.9) 149(14.6) Reference Sexually Transmitted Disease Yes 7 (0.6) 6(0.5) 1(0.0) 1.060 0.115 9.803 0.959 No 1011 (99.3) 860(84.4) 151(14.8) Reference Hypertension Yes 39(3.8) 31(3.0) 8(0.7) 1.317 0.554 3.133 0.533 No 979 (96.1) 835(82.0) 144(14.1) Reference Diabetes Yes 81 (7.9) 71(6.9) 10(0.9) 1.130 0.501 2.549 0.769 No 937(92.0) 795(78.0) 142(13.9) Reference Thyroid disorder Yes 22 (2.1) 18(1.7) 4(0.3) 1.962 0.596 6.456 0.267 No 996 (97.8) 848(83.3) 148(14.5) Reference Age at first pregnancy in group Nulligravida 15 (1.4) 15(1.4) 0(0)  30 years 104(10.2) 92(9.0) 12(1.1) Number of pregnancy in group No pregnancy 36(3.5) 29(2.8) 7(0.6) Reference Only 1 123(12.0) 101(9.9) 22(2.1) 0.496 0.173 1.418 0.191 Only 2 185 (18.5) 153(15.0) 32(3.1) 0.503 0.182 1.388 0.185 3 or more pregancy 674(66.2) 583 (57.2) 91(8.9) 0.352 0.133 0.928 0.035* Age of first intercourse in groups Less than 15 years 53 (5.2) 38(3.7) 15(1.4) Reference 16 to 20 years 216 (21.2) 176(17.2) 40(3.9) 0.497 0.229 1.077 0.076 21 to 25 years 469(46.0) 411(40.3) 58(5.6) 0.313 0.137 0.714 0.006* 26 to 30 years 169 (16.6) 142(13.9) 27(2.6) 0.315 0.123 0.804 0.016* 31 years and above 111 (10.9) 99(9.7) 12(1.1) 0.268 0.08 0.871 0.029* Number of sexual partner One person 906 (88.9) 773(75.9) 133(13.0) Reference More than one 112(11.0) 93(9.1) 19(1.8) 1.422 0.788 2.568 0.243 Ingestion of contraceptive pills Yes 436 (42.8) 387(38.0) 48 (4.7) 0.604 0.399 0.915 0.017* No 583(57.2) 479(47.0) 103(10.11) Reference Use of Condom Yes 18(1.7) 15(1.4) 4(0.39) 0.736 0.208 2.599 0.634 No 999(98.1) 851(83.5) 148 (14.5) Reference Use of Copper-T/Intrauterine Device (IUD) Yes 37 (3.6) 31(3.0) 6(0.5) 1.015 0.395 2.609 0.976 No 981 (96.3) 835(82.0) 146(14.3) Reference *Statistically significant; Cl = Confidence interval; OR  1 risk factor; OR = 1 no difference in the groups Clinical features and reproductive characteristics. ( n =1018) *Statistically significant; Cl = Confidence interval; OR  1 risk factor; OR = 1 no difference in the groups One hundred and fifty-two samples that were positive for HPV DNA were further tested for twenty genotypes. The most frequently identified HPV genotype was genotype 16 (26.97%), followed by HPV genotype 18 (17.11%). The other HPV types detected were HPV 31 and 33 (7.24%), HPV 35 (6.58%), HPV 26 (5.9%), HPV 52 and 53 (5.26%), HPV 58 and 51 (3.95%), HPV 39,45 and 66 (3.9%), HPV 83 (2.6%), and HPV 56 and 72 (0.66%). HPV 6 and HPV 68 were not detected. Multiple HPV genotypes ( n  = 35, 23.4% out of 152) were also observed in the study, where the most common combinations were HPV genotypes 16 and 18 (28.5% out of 35).

The findings of this study offer valuable insights into HPV epidemiology in Mizoram in the suburban hilly state of northeastern India. This study highlights the complex interactions among demographic, lifestyle, and clinical factors assessing the risk of HPV infection. The significant presence of high-risk HPV genotypes, especially HPV-16 and HPV-18, highlight the urgent need for tailored interventions, including HPV DNA-based screening and gender-inclusive vaccination campaigns. Although India has introduced HPV vaccines, uptake remains low in this region, underscoring the need for awareness and access. Public health initiatives should prioritize addressing cultural practices, enhancing access to cervical cancer prevention services, and raising awareness to alleviate the HPV burden in this high-risk population. However, the study’s cross-sectional design conclusions about the persistence, clearance, or reinfection dynamics of HPV. The absence of longitudinal follow-up, along with exclusion of male participants, further limits the generalizability and depth of inference. Despite these limitations, enhanced research and public health efforts may contribute significantly to reducing the HPV burden and cervical cancer incidence in this underserved region.

This study contributes to the understanding of the epidemiology of human papillomavirus in indigenous women residing in Mizoram. It is influenced by various sociodemographic factors, such as lifestyle, dietary habits, and cultural practices, and other health risk habits, such as the consumption of betel nuts and tobacco (chewing and smoking) and the intake of alcohol, are potential risks. Although the incidence of HPV is high in India, comprehensive population-based studies on its prevalence and genotype distribution are scarce. To our knowledge, this study is the first to investigate the prevalence and genotypic distribution of HPV among Mizo women on a larger scale. Mizoram is one of the seven northeastern states of India, sharing three state borders with Tripura, Assam and Manipur and two international borders in the west with Bangladesh and east with Myanmar. Its unique sociocultural and geographic features make it a key area for studies on public health and biodiversity, along with other research areas. According to the most recent report of the National Cancer Registry Programme, Mizoram has the highest rate of cervical cancer, and a 2.1% annual percentage change was reported in the state [ 21 ]. The current study population consisted of 1018 women, with the majority falling within the 41–50 years age group (35.3%). This age group has a relatively high prevalence of HPV infection, which aligns with the global pattern in which women of advanced age are relatively likely to be infected by HPV. However, contrasting evidence from a global vaccine trial by Ferris et al. reported a higher HPV prevalence in younger women aged 24–34 years (20.0%) compared to those aged 34–45 years (12.7%), highlighting age-related variations in HPV infection dynamics across different populations [ 22 ]. The current study exhibits significant geographic and occupational trends, with most participants originating from Aizawl, the state capital [ 23 ], suggesting that urbanization may influence access to healthcare services and participation in screening programs. Additionally, a higher prevalence of HPV was observed among public employees (9.8%). While the occupational category itself may not be a direct biological risk factor, this association could potentially reflect the impact of stress, underlying lifestyle or proactive healthcare-seeking behavior linked to nature within this occupational group. Consumption of tobacco and alcohol increase epithelial permeability, enhancing the ability of HPV to infect cells [ 24 ]. Moreover, the persistent irritation caused by betel nut chewing intensifies inflammation and creates a favorable environment for HPV-driven malignancies [ 24 ]. A similar study conducted in neighboring states reported that alcohol consumption, tobacco chewing and other risk factors were significantly associated with an increased risk of HPV infection, which aligns with the findings of the present study [ 25 ]. Chronic pelvic pain, though nonspecific, might signal persistent HPV infection or early cervical pathology. Reproductive history has been shown to influence the risk of HPV infection. Factors such as early age at first sexual intercourse, multiple sexual partners, high parity (number of full-term pregnancies), and contraceptive use are associated with HPV acquisition and persistence [ 23 , 26 ]. Study suggest that women with three or more pregnancies presented increased odds of infection, indicating that increased parity may weaken cervical tissue and increase the likelihood of harboring the virus [ 27 ]. Contraceptive practices, particularly the use of oral contraceptives (OC), remain among the most common forms of birth control. In the present study, women who reported using oral contraceptive pills were significantly less likely to be HPV positive than non-users (OR = 0.604, 95% CI: 0.399–0.915; p  = 0.017), suggesting a protective association. While this finding may initially appear to contrast with some reports linking long-term OC use to increased cervical cancer risk, existing literature acknowledges that the relationship may depend on the duration and biological context of use. For instance, Delgado-Rodriguez et al. observed that prolonged use of OCs may increase HPV persistence and alter cervical epithelial cells, potentially acting as an initiator of carcinogenesis. Thus, the protective effect observed in the present study may reflect shorter-term or regulated OC use, warranting further investigation into duration-dependent risk dynamics. [ 27 , 28 ] The early detection of precancerous lesions often fails in developing countries, despite the use of multiple techniques, leading many women to present with advanced stages of the disease. This issue arises from limited access to screening programs, a lack of awareness, and inadequate healthcare infrastructure [ 23 ]. A study reports that HPV DNA testing is more sensitive and specific compared with Pap cytology and VIA [ 28 ]. While others studies have shown that combining these methods enhances the ability to identify both HPV infection and abnormal cervical cells, improving the accuracy of early detection and prevention efforts which aligns with our study [ 29 ]. The most prevalent HPV genotype identified in this investigation was HPV-16 and HPV-18, which mirrors the regional and global dominance of high-risk genotypes in the etiology of cervical cancer [ 30 – 32 ]. The coexistence of multiple genotypic infections ranging from 2 to 4 was also observed among positive samples. Other researchers reported that multiple genotype infections occur randomly due to chance, growing evidence suggests they are significantly influenced by behavioral factors such as number of sexual partners and potentially by immunological mechanisms [ 33 ]. A large study by Chaturvedi et al. demonstrated that multiple HPV infections occur more frequently than expected under a Poisson distribution, suggesting non-random acquisition. Their findings indicate that although coinfecting genotypes appear to act independently in causing disease, their occurrence is likely driven by shared modes of transmission and host immune status, such as immunosuppression or smoking. This aligns with our findings and underscores the need to evaluate co-infection not only epidemiologically but also biologically in terms of disease progression and vaccine design [ 33 ]. Documents have shown that genotypes, particularly the combination of HPV-16 and HPV-18, amplify oncogenic potential, warranting further investigation into their clinical implications [ 34 ]. Firstly, the limitation of the study is that it is a cross-sectional study in nature. Secondly, the exclusive enrolment of female participants may introduce selection bias and reduce the generalizability. Behavioral and hygienic practices—including alcohol use, tobacco consumption, and smoking—were self-reported by participants, posing potential recall or reporting biases. Additionally, resource constraints, especially in low-incidence districts, restrict broader sampling and may have influenced detection rates. Despite these limitations, this study represents the first comprehensive investigation into the prevalence of HPV in this relatively understudied part of India, laying the groundwork for future research initiatives in the region.

The present cross-sectional study was conducted from November 2023-November 2024 at Viral Research and Diagnostic Laboratory, Department of Microbiology, Zoram Medical College, a tertiary care hospital at Falkawn, Mizoram, India. Approval was obtained from the Institutional Ethics Committee of Zoram Medical College, Mizoram No. F.20,016/1/18-ZMC/IEC/89. The study is also in accordance with the principle of the Declaration of Helsinki. After approval was obtained, the samples were collected from women of the same age group (20–73 years) who had visited the Gynecology Department from public and private hospitals in and around the suburban state of the city of Aizawl. Prior to enrollment, the participants were asked to provide informed consent and were informed of the potential advantages and disadvantages of the research. Other demographic details, such as age, occupation, education, social status, lifestyle, marital status, and clinical conditions, were obtained via a questionnaire before the collection of clinical samples. See supplementary material 1. The present study also included unmarried women who presented signs and symptoms related to the study objectives. Cervical specimens were obtained during pelvic examinations by physicians to obtain the consent of individuals. The cervix was examined via Cusco’s speculum for complete visualization. All the samples were collected using a sterile cervical brush or swab, placed in viral transport medium (VTM) and transported in a cold chain to the Viral Research and Diagnostic Laboratory (VRDL), Falkawn, for further investigation. Cervical specimens collected in the VTM were directly used for extracting DNA. The extraction of viral DNA was performed using QIAamp DNA Mini Kit according to the manufacturer’s instructions. The extracted DNA was stored at −20 °C until further testing. In this study, qualitative PCR was performed in CFX96 Bio-Rad thermocycler. The samples were first subjected to amplification in 20 reaction volumes via the consensus primers MY09/MY11 [ 17 ] and GP5+/GP6+ [ 18 ] with target sizes of 450 bp and 150 bp, respectively. See supplementary material 2. The MY09/MY11 and GP5+/GP6 + primers were chosen for their ability to amplify conserved regions of the HPV L1 gene, allowing broad detection of multiple HPV genotypes. MY09/MY11 target a ~ 450 bp region, while GP5+/GP6 + amplify a shorter ~ 150 bp fragment, improving sensitivity in samples with low viral load. Their combined use enhances overall detection accuracy and is well-established in epidemiological studies. All reagents were kept constant throughout the protocol, and each reaction containing approximately 100–200 ng of DNA, 8 µl of pre- ready-made 10x PCR master mix (Takara, Shiga, Japan) and 10 pmol of each primer was set up for the first PCR cycle. The PCR cycling parameters were as follows: initial denaturation at 95 °C for 5 min, followed by denaturation at 95 °C for 1 min, annealing at 53 °C for 1 min, elongation at 72 °C for 1 min, 30 amplification cycles, and a final extension at 72 °C for 4 min. The amplicons were analyzed using 2% agarose gel electrophoresis, and the products were stained with ethidium bromide, observed under UV light, and documented using Biorad GelDoc Go System. The positive HPV samples were genotyped using 20 HPV types, including low-risk (6, 11) and high-risk (16, 18,26, 31, 33, 35, 39, 45, 51, 52, 53, 56, 58, 59, 66, 68–73 and 82) types. See supplementary material 2. The PCRs for genotyping were performed with few modifications by Şahiner et al. [ 19 , 20 ] Descriptive analysis was performed for qualitative assessment in the study. A comparison of HPV positivity across various explanatory variables was done performed using simple logistic regression model in which the odds ratio was estimated with 95% confidence intervals. The p value < 0.05 was considered to indicate statistical significance. Cytology reports such as pap smear and their associations with HPV positivity were evaluated chi-square test. All estimates were examined by using IBM SPSS Statistics, version 22.

The causative agent of cervical cancer, human papillomavirus (HPV), is a significant public health concern globally. HPV is transmitted primarily through sexual contact and infects both males and females. The majority of the virus’s clinical manifestations, ranging from benign warts to malignancies, are caused by epithelial cell infection [ 1 ]. At some time in their life, more than 80% of those who engage in copulation contract HPV [ 2 ]. There are over 200 different types of HPV, categorized into low-risk and high-risk types on the basis of their potential to cause cancer. Low-risk types (e.g., HPV 6 and 11) are associated with genital warts, whereas high-risk types (e.g., HPV 16 and 18) are linked to various cancers, most notably cervical cancer [ 3 , 4 ]. However, other high-risk genotypes such as HPV 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 66, and 68 also play critical roles in carcinogenesis and are included in broad-spectrum vaccines like the nonavalent HPV vaccine (Gardasil 9). This vaccine covers nine genotypes: 6, 11, 16, 18, 31, 33, 45, 52, and 58, thereby extending protection against approximately 90% of cervical cancers [ 5 ]. HPV is primarily transmitted through skin-to-skin genital contact, with early sexual debut, multiple partners, and immature cervical epithelium increasing susceptibility. Although nonsexual transmission (e.g., vertical during childbirth) is rare, it is possible. Females are more frequently infected, though both sexes can develop HPV-related cancers. Immunocompromised individuals, such as those with HIV, are more prone to persistent infection and related complications. Vaccination and routine cervical screening (e.g., Pap smears and HPV DNA testing) remain critical for early detection and prevention [ 3 , 5 – 7 ]. The prevalence of HPV in patients with cervical cancer varies globally, with higher rates in regions with limited access to healthcare and cervical cancer screening such as Pap smears [ 8 ]. Nearly all cervical cancer cases are attributed to persistent infections with high-risk HPV types, with HPV-16 and HPV-18 accounting for approximately 70% of cases worldwide. These two genotypes are recognized as the most oncogenic among the high-risk HPV types, contributing to a significant burden of cervical cancer worldwide [ 6 ]. Other HPV-associated cancers include oropharyngeal cancer, anal cancer, penile cancer, vaginal cancer, etc [ 3 ]. According to the most recent GLOBOCAN estimates, in 2022, there were approximately 662,301 new cervical cancer cases and 348,709 deaths worldwide [ 9 ]. In Asia, the average HPV incidence among asymptomatic women with normal cervical cytology is 9.4%, whereas in Oceania, the prevalence is 30.9% [ 10 ]. According to the World Health Organization, India has high rates of HPV infections and HPV-related cancers, accounting for nearly one-quarter of the global burden [ 11 ]. Cervical cancer is the most significant health consequence of HPV, which ranks as the second leading cause of female cancer in India, with an estimated 123,907 new cervical cancer cases diagnosed annually. Cervical cancer is the second most common female cancer in women aged 15–44 years in India [ 12 ]. Few Indian studies have reported that the frequency of HPV infection ranges from 2.3 to 36.9%. There are few community-based studies from India that use polymerase chain reaction (PCR)-based techniques to test sexually active asymptomatic women [ 13 ]. In 2020, India accounted for 24% of all cancers linked to HPV, particularly HPV types 16 and 18, which are the causes of four of every five cervical cancer cases reported [ 14 ]. Mizoram, despite being the second least populated state in India, which is in the northeastern region, had the highest cervical cancer incidence in the nation (28/100,000 women between 2012 and 2014), which may be explained by the high HPV prevalence [ 15 , 16 ]. Understanding the epidemiology of HPV in India, especially in regions with distinct sociodemographic profiles such as Mizoram, is essential for devising effective prevention and control strategies. Therefore, this study was conducted to determine the epidemiology of HPV infection and its associated risk factors among women in Mizoram.

Supplementary Material 1. Supplementary Material 1. Supplementary Material 2. Supplementary Material 2.