Interactions between inflammatory gene polymorphisms and HTLV-I infection for total death, incidence of cancer, and atherosclerosis-related diseases among the Japanese population

• Published in: Journal of epidemiology Vol. 27; no. 9; pp. 420 - 427
• Main Authors: Kairupan, Tara Sefanya, Ibusuki, Rie, Kheradmand, Motahare, Sagara, Yasuko, Mantjoro, Eva Mariane, Nindita, Yora, Niimura, Hideshi, Kuwabara, Kazuyo, Ogawa, Shin, Tsumematsu-Nakahata, Noriko, Nerome, Yasuhito, Owaki, Tetsuhiro, Matsushita, Toshifumi, Maenohara, Shigeho, Yamaguchi, Kazunari, Takezaki, Toshiro
• Format: Journal Article
• Language: English
• Published: Japan Elsevier B.V 01.09.2017; Japan Epidemiological Association; Elsevier
• Subjects: Adult; Aged; Arteriosclerosis; Atherosclerosis; Atherosclerosis - complications; Atherosclerosis - genetics; Cancer; Cohort Studies; Confidence intervals; Death; Diseases; Etiology; Female; Gene polymorphism; HTLV-I; HTLV-I Infections - genetics; HTLV-I Infections - mortality; Humans; Incidence; Infections; Inflammation; Interaction; Interleukin 10; Interleukin-10 - genetics; Japan - epidemiology; Male; Middle Aged; Mortality; Neoplasms - epidemiology; Neoplasms - genetics; NF-kappa B p50 Subunit - genetics; Original; Polymorphism; Polymorphism, Genetic; Population; Population studies; Risk factors; Statistical analysis; Tumor necrosis factor; Tumor Necrosis Factor-alpha - genetics; Viruses; Japan; HTLV-I; Inflammation; Gene polymorphism; Interaction
• ISSN: 0917-5040; 1349-9092
• DOI: 10.1016/j.je.2016.08.017

An increased risk of total death owing to human T-lymphotropic virus type-I (HTLV-I) infection has been reported. However, its etiology and protective factors are unclear. Various studies reported fluctuations in immune-inflammatory status among HTLV-I carriers. We conducted a matched cohort study among the general population in an HTLV-I-endemic region of Japan to investigate the interaction between inflammatory gene polymorphisms and HTLV-I infection for total death, incidence of cancer, and atherosclerosis-related diseases. We selected 2180 sub-cohort subjects aged 35–69 years from the cohort population, after matching for age, sex, and region with HTLV-I seropositives. They were followed up for a maximum of 10 years. Inflammatory gene polymorphisms were selected from TNF-α, IL-10, and NF-κB1. A Cox proportional hazard model was used to estimate the hazard ratio (HR) and the interaction between gene polymorphisms and HTLV-I for risk of total death and incidence of cancer and atherosclerosis-related diseases. HTLV-I seropositivity rate was 6.4% in the cohort population. The interaction between TNF-α 1031T/C and HTLV-I for atherosclerosis-related disease incidence was statistically significant (p = 0.020). No significant interaction was observed between IL-10 819T/C or NF-κB1 94ATTG ins/del and HTLV-I. An increased HR for total death was observed in the Amami island region, after adjustment of various factors with gene polymorphisms (HR 3.03; 95% confidence interval, 1.18–7.77). The present study found the interaction between TNF-α 1031T/C and HTLV-I to be a risk factor for atherosclerosis-related disease. Further follow-up is warranted to investigate protective factors against developing diseases among susceptible HTLV-I carriers. •We observed death and incidence risk with HTLV-I and SNPs in a matched cohort study.•An increased risk for total death with HTLV-I was observed in the island region.•Inflammatory SNP interacted with HTLV-I for atherosclerosis-related disease risk.