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Human papillomavirus (HPV) is a circular double-stranded DNA virus capable of infecting skin and mucous membranes and is a sexually transmitted infection (STI) with universal incidence. High-risk HPVs induce cell transformations that can progress to carcinoma in situ and cervical cancer in more than 99% of cases. The development of these lesions is associated with infection persistence which may be determined by individual intrinsic factors, such as genetic polymorphisms. It has been reported that apolipoprotein B mRNA editing enzyme catalytic polypeptide like (APOBEC), plays an important role in diverse vital biological processes including immunity, gene expression regulation and viral restriction including HPV through the deamination of cytidines. This enzyme gene may present a 30-kb deletion polymorphism, generating a hybrid transcript, formed by the translated region of APOBEC3A and the 3' untranslated region (UTR) of APOBEC3B, known as APOBEC3A/B, capable of influencing the viral infection and its consequences. The objective of this work is to evaluate the APOBEC3A/B deletion polymorphism influence in HPV infection. The experiments were carried out with samples obtained from female patients over the age of 18 years, after the ethics committee of the Londrina State University approval (CAAE 05505912.0.0000.5231). A total of 418 samples were analyzed, 226 samples from HPV negative patients were allocated in the control group and 192 samples from HPV positive patients int the experimental group. The samples were submitted to DNA extraction using the salting out method, the APOBEC3A/B polymorphism analysis was carried out by the allele-specific PCR technique, followed by statistical analysis. The chi-square test was applied to compare the genotype proportion between groups. P-values <0.05 were considered statistically significant. The genotypes frequency in the control group was 69.03% (156) wild-type homozygote, 27.43% (62) heterozygous and 3.54% (8) deleted homozygotes. In the experimental group, the frequency of observed genotypes was 68.23% (131) wild-type homozygote, 27.60% (53) heterozygote and 4.17% (8) deleted homozygotes. There was no significant difference in the genotypes frequency (P=0.94) between the control and the experimental groups. Further analyses are necessary to confirm the presented results, since the study of the APOBEC3A/B polymorphism is important in the understanding of the mechanisms underlying HPV infection.
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