Polymorphism in the promoter region of the Toll-like receptor 9 gene and cervical human papillomavirus infection

Imagem de Miniatura
Arquivos
art_VILLA_Polymorphism_in_the_promoter_region_of_the_Toll_2013.PDF (198.71 KB)
Citações na Scopus
16
Tipo de produção
article
Data de publicação
2013
DOI
Scopus
Web of Science
PubMed
Título da Revista
ISSN da Revista
Título do Volume
Editora
SOC GENERAL MICROBIOLOGY
Autores
OLIVEIRA, Lucas Boeno
LOUVANTO, Karolina
RAMANAKUMAR, Agnihotram V.
FRANCO, Eduardo L.
Citação
JOURNAL OF GENERAL VIROLOGY, v.94, p.1858-1864, 2013
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Polymorphism in the Toll-like receptor (TLR) 9 gene has been shown to have a significant role in some diseases; however, little is known about its possible role in the natural history of human papillomavirus (HPV) infections. We investigated the association between a single-nucleotide polymorphism (SNP) (rs5743836) in the promoter region of TLR9 (T1237C) and type-specific HPV infections. Specimens were derived from a cohort of 2462 women enrolled in the Ludwig McGill Cohort Study. We randomly selected 500 women who had a cervical HPV infection detected at least once during the study as cases. We defined two control groups: (i) a random sample of 300 women who always tested HPV negative, and (ii) a sample of 234 women who were always HPV negative but had a minimum of ten visits during the study. TLR9 genotyping was performed using bidirectional PCR amplification of specific alleles. Irrespective of group, the WT homozygous TLR9 genotype (TT) was the most common form, followed by the heterozygous (TO) and the mutant homozygous (CC) forms. There were no consistent associations between polymorphism and infection risk, either overall or by type or species. Likewise, there were no consistently significant associations between polymorphism and HPV clearance or persistence. We concluded that this polymorphism in the promoter region of TLR9 gene does not seem to have a mediating role in the natural history of the HPV infection.
Palavras-chave
URI
https://observatorio.fm.usp.br/handle/OPI/4012
Referências
  1. Carvalho A, 2012, GENES IMMUN, V13, P197, DOI 10.1038/gene.2011.59
  2. Carvalho A, 2011, PLOS ONE, V6
  3. Carvalho A, 2008, J INFECT DIS, V197, P618, DOI 10.1086/526500
  4. Corr SC, 2009, J INNATE IMMUN, V1, P350, DOI 10.1159/000200774
  5. Daud II, 2011, INT J CANCER, V128, P879, DOI 10.1002/ijc.25400
  6. Franco E, 1999, Rev Panam Salud Publica, V6, P223, DOI 10.1590/S1020-49891999000900001
  7. HALLORAN ME, 1995, EPIDEMIOLOGY, V6, P142, DOI 10.1097/00001648-199503000-00010
  8. Hasan UA, 2007, J IMMUNOL, V178, P3186
  9. Hasimu Ayshamgul, 2011, Chin J Cancer, V30, P344
  10. Lazarus R, 2003, GENOMICS, V81, P85, DOI 10.1016/S0888-7543(02)00022-8
  11. Lee JW, 2007, MOL CARCINOGEN, V46, P941, DOI 10.1002/mc.20325
  12. Lu KC, 2011, TOHOKU J EXP MED, V225, P109, DOI 10.1620/tjem.225.109
  13. Mahmud SM, 2007, J INFECT DIS, V196, P82, DOI 10.1086/518612
  14. Misch EA, 2008, CLIN SCI, V114, P347, DOI 10.1042/CS20070214
  15. Netea MG, 2012, NAT IMMUNOL, V13, P535, DOI 10.1038/ni.2284
  16. Ng MTH, 2010, INFECT IMMUN, V78, P1345, DOI 10.1128/IAI.01226-09
  17. Novak N, 2007, ALLERGY, V62, P766, DOI 10.1111/j.1398-9995.2007.01358.x
  18. Pandey S, 2011, MOL BIOL REP, V38, P4715, DOI 10.1007/s11033-010-0607-z
  19. Rabachini T, 2010, BMC GENET, V11, DOI 10.1186/1471-2156-11-44
  20. Rosa MI, 2012, ARCH GYNECOL OBSTET, V285, P143, DOI 10.1007/s00404-011-1925-7
  21. Roszak A, 2012, MOL BIOL REP, V39, P8425, DOI 10.1007/s11033-012-1695-8
  22. Schlecht NF, 2001, JAMA-J AM MED ASSOC, V286, P3106, DOI 10.1001/jama.286.24.3106
  23. Trottier Helen, 2006, Vaccine, V24 Suppl 1, pS1
  24. Vandermark ER, 2012, VIROLOGY, V425, P53, DOI 10.1016/j.virol.2011.12.023
  25. Weng YJ, 2011, J HUAZHONG U SCI-MED, V31, P550, DOI 10.1007/s11596-011-0488-y

Coleções
Artigos e Materiais de Revistas Científicas - FM/MDR
Artigos e Materiais de Revistas Científicas - LIM/24