{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,13]],"date-time":"2026-02-13T09:14:16Z","timestamp":1770974056825,"version":"3.50.1"},"reference-count":45,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2008,10,21]],"date-time":"2008-10-21T00:00:00Z","timestamp":1224547200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Medical Virology"],"published-print":{"date-parts":[[2008,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>HTLV\u20101 is the etiologic agent of ATL and HAM\/TSP. The majority of HTLV\u20101\u2010infected individuals remain asymptomatic, indicating that the infection alone is not sufficient to cause the diseases. It has been reported that cytokine gene polymorphisms, including polymorphisms at IL\u20106 and IL\u201010 gene, might be important. We analyzed SNP in the promoter region of the IL\u20106: \u2212174, \u2212572, \u2212597, and \u2212634 positions, and IL\u201010: \u2212592 position to evaluate the role of these polymorphisms in the HAM\/TSP pathogenesis in 133 HTLV\u20101 infected individuals and in 100 healthy individuals from Salvador, Bahia, Brazil. The \u2212634C allele frequencies were higher among HAM\/TSP patients (21.2%) than among oligosymptomatic (6.5%; <jats:italic>P<\/jats:italic>\u2009=\u20090.038) and asymptomatic (9.5%; <jats:italic>P<\/jats:italic>\u2009=\u20090.025) subjects. Similarly, the \u2212174G allele frequencies were higher in HAM\/TSP patients than in oligosymptomatic patients (<jats:italic>P<\/jats:italic>\u2009=\u20090.02). Moreover, the \u2212634GC\/\u2212174GG genotype combination was identified at a higher frequency (38.5%) in the HAM\/TSP patients than in subjects with other clinical status (8.7%; <jats:italic>P<\/jats:italic>\u2009=\u20090.016 for oligosymptomatic and 15.5%, <jats:italic>P<\/jats:italic>\u2009=\u20090.012 for asymptomatic patients). However, the multivariate logistic regression including the genotypes of the three studied loci showed that only \u2212634 C IL\u20106 carriers remain as significant and independent TSP\/HAM predictor (odds ratio [OR]\u2009=\u20095.31; 95% [CI]\u2009=\u20091.60\u201317.56; <jats:italic>P<\/jats:italic>\u2009=\u20090.006). We suggest that \u2212634 G C in IL\u20106 could contribute to HAM\/TSP development and that identification of the collective influence of several cytokine polymorphisms, their prevalence, and their interaction could help to better understand this disease. J. Med. Virol. 80:2141\u20132146, 2008. \u00a9 2008 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jmv.21341","type":"journal-article","created":{"date-parts":[[2008,10,21]],"date-time":"2008-10-21T13:54:44Z","timestamp":1224597284000},"page":"2141-2146","source":"Crossref","is-referenced-by-count":19,"title":["Correlation between polymorphisms at interleukin\u20106 but not at interleukin\u201010 promoter and the risk of human T lymphotropic virus type I\u2010associated myelopathy\/tropical spastic paraparesis in Brazilian individuals"],"prefix":"10.1002","volume":"80","author":[{"given":"Sandra Rocha","family":"Gadelha","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Luiz Carlos","family":"Junior Alc\u00e2ntara","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gisele 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