IFN-gamma and IL-12B polymorphisms in women with cervical intraepithellial neoplasia caused by human papillomavirus

• DOI: 10.1007/s11033-012-1597-9
• Publication Date: 2012-02-11T03:48:41Z
• Authors: Viviane do Carmo ...; Jamilly Lopes de ...; Camilla Albertina...; Maria da Conceiçã...; Sandra de Andrade...; Melânia Amorim; Maria de Mascena ...; Ana Lúcia Figueir...; Paulo Roberto Ele...
• Keywords: 0303 health sciences; Genotype; Interleukin-12 Subunit p40; Papillomavirus Infections; Uterine Cervical Neoplasms; Alphapapillomavirus; Uterine Cervical Dysplasia; Polymorphism, Single Nucleotide; 3. Good health; Interferon-gamma; 03 medical and health sciences; Humans; Female

The Human Papillomavirus (HPV) is a sexually transmitted organism associated with Cervical Intraepithelial Neoplasia (CIN) and cervical cancer, the second main cause of malignancy in women worldwide. The virus itself, however, is not enough to cause lesions on the cervix. Several studies suggest that some polymorphic sites changes the cytokines levels and influence the cancer development in HPV infected patients. In this study, we evaluated the presence of functional polymorphisms at +874 (T/A) IFNG and +1188 (A/C) IL-12B genes in cervical smears samples from 76 healthy women and 162 women, HPV positive, with CIN lesion--CIN I (45), CIN II (55), CIN III (53) and cervical cancer (9)--in Brazilian population. There was no significant differences in genotype (p = 0.4192) and allele (p = 0.370; OR = 1.20) distributions between CIN patients and control groups on IFNG allelic polymorphism. Moreover, for IL-12B gene, there was a significant difference in genotype (p = 0.015) and allele distribution (p = 0.014; OR = 0.5754) between the groups. When samples were stratified according to grade of cervical lesion, the AA genotype and A allele were less frequent in the group with low-grade cervical lesions than in group with high-grade cervical lesions (p = 0.0036 and p = 0.0010; OR = 0.3819, respectively), suggesting that the C allele (mutant) may protect against the emergence of CIN lesions and its progression.