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April 24, 2026SHILAP Revista de lepidopterología0 citationsOpen Access

TP53 codon 47 and 72 polymorphisms show no association with HPV in Zimbabwean women living with HIV and histologically confirmed cervical and vulvar disease

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OKOppah KuguyoUniversity of Cape TownMPMargaret PascoeELEugénie LohmannCentre international de recherche sur le cancer

Key Points

  • This study investigates the relationship between TP53 codon polymorphisms and HPV in women living with HIV.
  • Cross-sectional design involving 102 women living with HIV over 18 years old with confirmed cervical or vulvar disease.
  • Tissue biopsies analyzed for HPV genotypes using ATILA multiplex system and TP53 variants through Sanger sequencing.
  • Logistic regression used to assess associations between HPV genotypes and TP53 variants.
  • Cervical cancer and intraepithelial neoplasia classifications were reported with various proportions.
  • HPV16 prevalence was significant at 40% in vulvar tissue.
  • No significant association was found between TP53 codon 72 and 47 mutations and HPV genotypes (p > 0.05).

Abstract

Introduction Interaction between HIV and human papillomavirus (HPV) increases the risk of HPV persistence. However, a few studies have explored the interplay between host genetic factors and HPV in women living with HIV (WLWH). We report on a study investigating the role of TP53 mutations among HPV DNA-positive cervical and vulvar tissue from Zimbabwean WLWH. Methods This cross-sectional study recruited 102 WLWH aged over 18 years, with histologically confirmed vulvar ( n = 13) or cervical disease ( n = 89). Vulvar or cervical tissue biopsies, preserved in formalin-fixed paraffin-embedded (FFPE) blocks, were retrieved. Tumour DNA was extracted and analyzed for 17 HPV genotypes using the ATILA multiplex system. The DNA was also examined for TP53 variants located in codon 72 and 47 using Sanger sequencing. Associations between HPV genotypes and TP53 variants were assessed using logistic regression. Results The histological classifications had the following proportions: cervical intraepithelial neoplasia (CIN)1: 10%, CIN2: 4.5%, CIN3: 82%, and cervical cancer: 3.4%. Vulvar disease was classified as: vulvar intraepithelial neoplasia (VIN)3: 84.6%, and vulvar cancer (15.4%). HPV16 prevalence was 40% and 64% in vulvar tissue. Codon 72G and codon 47 T alleles had frequencies of 34.1% and 2.9% in cervical tissue, and 29.2% and 4.2% in vulvar tissue, respectively. There was no significant association between TP53 codon 72 and 47 mutations, and HPV genotypes ( p 0.05). Discussion and Conclusion These findings underscore the need to conduct further research to identify other genetic variants within the TP53 gene that may contribute to the role of TP53 in HPV susceptibility that has been previously reported in other studies.

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Cite This Study

Kuguyo et al. (2026) studied this question.

synapsesocial.com/papers/69eb07a4553a5433e34b325ahttps://doi.org/10.3389/frph.2026.1808566
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