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

Tara Sefanya Kairupan, Rie Ibusuki, Motahare Kheradmand, Yasuko Sagara, Eva Mariane Mantjoro, Yora Nindita, Hideshi Niimura, Kazuyo Kuwabara, Shin Ogawa, Noriko Tsumematsu-Nakahata, Yasuhito Nerome, Tetsuhiro Owaki, Toshifumi Matsushita, Shigeho Maenohara, Kazunari Yamaguchi, Toshiro Takezaki

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Background: 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. Method: 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. Results: HTLV-I seropositivity rate was 6.4% in the cohort population. The interaction between TNF-a 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). Conclusion: 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.

Original languageEnglish
Pages (from-to)420-427
Number of pages8
JournalJournal of Epidemiology
Volume27
Issue number9
DOIs
Publication statusPublished - 2017

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Virus Diseases
Atherosclerosis
Incidence
Viruses
Population
Genes
Neoplasms
Interleukin-10
Human T-lymphotropic virus 1
Proportional Hazards Models
Islands
Japan
Cohort Studies
Confidence Intervals

Keywords

  • Gene polymorphism
  • HTLV-I
  • Inflammation
  • Interaction

ASJC Scopus subject areas

  • Epidemiology

Cite this

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

In: Journal of Epidemiology, Vol. 27, No. 9, 2017, p. 420-427.

Research output: Contribution to journalArticle

Kairupan, TS, Ibusuki, R, Kheradmand, M, Sagara, Y, Mantjoro, EM, Nindita, Y, Niimura, H, Kuwabara, K, Ogawa, S, Tsumematsu-Nakahata, N, Nerome, Y, Owaki, T, Matsushita, T, Maenohara, S, Yamaguchi, K & Takezaki, T 2017, 'Interactions between inflammatory gene polymorphisms and HTLV-I infection for total death, incidence of cancer, and atherosclerosis-related diseases among the Japanese population', Journal of Epidemiology, vol. 27, no. 9, pp. 420-427. https://doi.org/10.1016/j.je.2016.08.017
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. / Interactions between inflammatory gene polymorphisms and HTLV-I infection for total death, incidence of cancer, and atherosclerosis-related diseases among the Japanese population. In: Journal of Epidemiology. 2017 ; Vol. 27, No. 9. pp. 420-427.
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abstract = "Background: 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. Method: 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. Results: HTLV-I seropositivity rate was 6.4{\%} in the cohort population. The interaction between TNF-a 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). Conclusion: 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.",
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T1 - Interactions between inflammatory gene polymorphisms and HTLV-I infection for total death, incidence of cancer, and atherosclerosis-related diseases among the Japanese population

AU - Kairupan, Tara Sefanya

AU - Ibusuki, Rie

AU - Kheradmand, Motahare

AU - Sagara, Yasuko

AU - Mantjoro, Eva Mariane

AU - Nindita, Yora

AU - Niimura, Hideshi

AU - Kuwabara, Kazuyo

AU - Ogawa, Shin

AU - Tsumematsu-Nakahata, Noriko

AU - Nerome, Yasuhito

AU - Owaki, Tetsuhiro

AU - Matsushita, Toshifumi

AU - Maenohara, Shigeho

AU - Yamaguchi, Kazunari

AU - Takezaki, Toshiro

PY - 2017

Y1 - 2017

N2 - Background: 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. Method: 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. Results: HTLV-I seropositivity rate was 6.4% in the cohort population. The interaction between TNF-a 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). Conclusion: 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.

AB - Background: 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. Method: 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. Results: HTLV-I seropositivity rate was 6.4% in the cohort population. The interaction between TNF-a 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). Conclusion: 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.

KW - Gene polymorphism

KW - HTLV-I

KW - Inflammation

KW - Interaction

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