Background Community-based HPV genotype data remain limited in southern Vietnam, where screening programmes must interpret genotype-specific risk in a population with low documented HPV vaccination. We described HPV prevalence, IARC Group 1 carcinogenic genotype distribution, infection multiplicity, and woman-level detection of HPV16/18 and of at least one genotype included in the nonavalent vaccine. Methods From January to June 2026, we conducted a community-based cross-sectional study among 1,193 enrolled ever-married women aged 25–65 years in Ca Mau Province, Vietnam; the response-rate denominator was 1,565 women, yielding a response rate of 76.2%. A three-stage sampling design with random selection procedures was used. Because stage-specific selection probabilities were unavailable, prevalence estimates are reported as unweighted descriptive proportions. Cervical specimens were tested by real-time PCR for 23 HPV genotypes, and cervical cytology was performed concurrently. Crude proportions and Wilson 95% confidence intervals (CIs) calculated under a simple-random-sampling assumption are reported; no inferential comparisons were performed. Results Crude, unweighted HPV prevalence was 7.1% (85/1,193; 95% CI 5.8–8.7); all 85 had a retrievable genotype result. Overall, 78 (91.8%) carried at least one manufacturer-designated high-risk genotype and 66 (77.6%) carried an IARC Group 1 carcinogenic genotype. HPV52 (20/85, 23.5%) and HPV58 (14/85, 16.5%) were the most frequently detected genotypes, followed by HPV16, HPV51 and HPV59 (each 10/85, 11.8%) and HPV18 (4/85, 4.7%); genotype frequencies were not compared statistically. Multiple genotypes were detected in 25/85 HPV-positive women (29.4%). Among women with an IARC Group 1 genotype, 52/66 (78.8%) had neither HPV16 nor HPV18. At least one nonavalent-vaccine genotype was detected in 50/85 HPV-positive women (58.8%). Conclusions Overall HPV prevalence was low, HPV52 and HPV58 were the most frequently detected genotypes, and nearly four in five women with an IARC Group 1 carcinogenic genotype carried neither HPV16 nor HPV18. Because stage-specific selection probabilities were unavailable, these are unweighted descriptive estimates for the study sample rather than design-based estimates for Ca Mau Province. They describe the baseline genotype distribution in a population with low documented HPV vaccination. Genotype frequency should not be translated into local triage policy without longitudinal evidence linking individual types to histologically confirmed precancer and cancer.
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