Contribution of Irf-1 promoter polymorphisms to the Th1-type cell response and interferon-β monotherapy for chronic hepatitis C

Hidetsugu Saito, Shinichiro Tada, Nobuhiro Nakamoto, Kumi Kitamura, Hiromi Horikawa, Satoshi Kurita, Hirotoshi Ebinuma, Hiromasa Ishii, Masahiko Takahashi, Shin Tanaka, Toshifumi Hibi

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

We recently reported promoter polymorphisms in the IRF-1 gene, an interferon-inducible gene that plays an important role in host antiviral function. The promoter activity was shown to be different between different polymorphisms. In this study, we investigated the relationship between IRF-1 promoter polymorphisms and the response to interferon monotherapy for chronic hepatitis C. Eighteen patients with a low initial viral load or hepatitis C virus (HCV) genotype non-1b received 6-months course of interferon-β monotherapy. IRF-1 gene mutations and the treatment response were investigated. The IRF-1 promoter type possessing a higher promoter activity (-415C/-410A/-300A) was found in only three patients, all of which had a lower viral load than those with other promoter types and were able to obtain a sustained viral response. Flow cytometric analysis of peripheral blood mononuclear cells showed that the patients with a higher promoter activity of the IRF-1 had a significantly higher proportion of T helper 1-type CD4+ cells after interferon administration than those of other promoter types. These results suggest that IRF-1 promoter polymorphisms may contribute, at least partially, to host antiviral activity for chronic hepatitis C.

Original languageEnglish
Pages (from-to)25-32
Number of pages8
JournalHepatology Research
Volume32
Issue number1
DOIs
Publication statusPublished - 2005 May

Fingerprint

Th1 Cells
Chronic Hepatitis C
Interferons
Viral Load
Antiviral Agents
Genes
Hepacivirus
Blood Cells
Genotype
Mutation
Therapeutics

Keywords

  • Host immunological activity
  • Interferon monotherapy
  • Interferon regulatory factor
  • Promoter polymorphims
  • Response

ASJC Scopus subject areas

  • Gastroenterology

Cite this

Contribution of Irf-1 promoter polymorphisms to the Th1-type cell response and interferon-β monotherapy for chronic hepatitis C. / Saito, Hidetsugu; Tada, Shinichiro; Nakamoto, Nobuhiro; Kitamura, Kumi; Horikawa, Hiromi; Kurita, Satoshi; Ebinuma, Hirotoshi; Ishii, Hiromasa; Takahashi, Masahiko; Tanaka, Shin; Hibi, Toshifumi.

In: Hepatology Research, Vol. 32, No. 1, 05.2005, p. 25-32.

Research output: Contribution to journalArticle

Saito, H, Tada, S, Nakamoto, N, Kitamura, K, Horikawa, H, Kurita, S, Ebinuma, H, Ishii, H, Takahashi, M, Tanaka, S & Hibi, T 2005, 'Contribution of Irf-1 promoter polymorphisms to the Th1-type cell response and interferon-β monotherapy for chronic hepatitis C', Hepatology Research, vol. 32, no. 1, pp. 25-32. https://doi.org/10.1016/j.hepres.2005.03.009
Saito, Hidetsugu ; Tada, Shinichiro ; Nakamoto, Nobuhiro ; Kitamura, Kumi ; Horikawa, Hiromi ; Kurita, Satoshi ; Ebinuma, Hirotoshi ; Ishii, Hiromasa ; Takahashi, Masahiko ; Tanaka, Shin ; Hibi, Toshifumi. / Contribution of Irf-1 promoter polymorphisms to the Th1-type cell response and interferon-β monotherapy for chronic hepatitis C. In: Hepatology Research. 2005 ; Vol. 32, No. 1. pp. 25-32.
@article{647f1949656741a9896f51787a6d5716,
title = "Contribution of Irf-1 promoter polymorphisms to the Th1-type cell response and interferon-β monotherapy for chronic hepatitis C",
abstract = "We recently reported promoter polymorphisms in the IRF-1 gene, an interferon-inducible gene that plays an important role in host antiviral function. The promoter activity was shown to be different between different polymorphisms. In this study, we investigated the relationship between IRF-1 promoter polymorphisms and the response to interferon monotherapy for chronic hepatitis C. Eighteen patients with a low initial viral load or hepatitis C virus (HCV) genotype non-1b received 6-months course of interferon-β monotherapy. IRF-1 gene mutations and the treatment response were investigated. The IRF-1 promoter type possessing a higher promoter activity (-415C/-410A/-300A) was found in only three patients, all of which had a lower viral load than those with other promoter types and were able to obtain a sustained viral response. Flow cytometric analysis of peripheral blood mononuclear cells showed that the patients with a higher promoter activity of the IRF-1 had a significantly higher proportion of T helper 1-type CD4+ cells after interferon administration than those of other promoter types. These results suggest that IRF-1 promoter polymorphisms may contribute, at least partially, to host antiviral activity for chronic hepatitis C.",
keywords = "Host immunological activity, Interferon monotherapy, Interferon regulatory factor, Promoter polymorphims, Response",
author = "Hidetsugu Saito and Shinichiro Tada and Nobuhiro Nakamoto and Kumi Kitamura and Hiromi Horikawa and Satoshi Kurita and Hirotoshi Ebinuma and Hiromasa Ishii and Masahiko Takahashi and Shin Tanaka and Toshifumi Hibi",
year = "2005",
month = "5",
doi = "10.1016/j.hepres.2005.03.009",
language = "English",
volume = "32",
pages = "25--32",
journal = "Hepatology Research",
issn = "1386-6346",
publisher = "Wiley-Blackwell Publishing Ltd",
number = "1",

}

TY - JOUR

T1 - Contribution of Irf-1 promoter polymorphisms to the Th1-type cell response and interferon-β monotherapy for chronic hepatitis C

AU - Saito, Hidetsugu

AU - Tada, Shinichiro

AU - Nakamoto, Nobuhiro

AU - Kitamura, Kumi

AU - Horikawa, Hiromi

AU - Kurita, Satoshi

AU - Ebinuma, Hirotoshi

AU - Ishii, Hiromasa

AU - Takahashi, Masahiko

AU - Tanaka, Shin

AU - Hibi, Toshifumi

PY - 2005/5

Y1 - 2005/5

N2 - We recently reported promoter polymorphisms in the IRF-1 gene, an interferon-inducible gene that plays an important role in host antiviral function. The promoter activity was shown to be different between different polymorphisms. In this study, we investigated the relationship between IRF-1 promoter polymorphisms and the response to interferon monotherapy for chronic hepatitis C. Eighteen patients with a low initial viral load or hepatitis C virus (HCV) genotype non-1b received 6-months course of interferon-β monotherapy. IRF-1 gene mutations and the treatment response were investigated. The IRF-1 promoter type possessing a higher promoter activity (-415C/-410A/-300A) was found in only three patients, all of which had a lower viral load than those with other promoter types and were able to obtain a sustained viral response. Flow cytometric analysis of peripheral blood mononuclear cells showed that the patients with a higher promoter activity of the IRF-1 had a significantly higher proportion of T helper 1-type CD4+ cells after interferon administration than those of other promoter types. These results suggest that IRF-1 promoter polymorphisms may contribute, at least partially, to host antiviral activity for chronic hepatitis C.

AB - We recently reported promoter polymorphisms in the IRF-1 gene, an interferon-inducible gene that plays an important role in host antiviral function. The promoter activity was shown to be different between different polymorphisms. In this study, we investigated the relationship between IRF-1 promoter polymorphisms and the response to interferon monotherapy for chronic hepatitis C. Eighteen patients with a low initial viral load or hepatitis C virus (HCV) genotype non-1b received 6-months course of interferon-β monotherapy. IRF-1 gene mutations and the treatment response were investigated. The IRF-1 promoter type possessing a higher promoter activity (-415C/-410A/-300A) was found in only three patients, all of which had a lower viral load than those with other promoter types and were able to obtain a sustained viral response. Flow cytometric analysis of peripheral blood mononuclear cells showed that the patients with a higher promoter activity of the IRF-1 had a significantly higher proportion of T helper 1-type CD4+ cells after interferon administration than those of other promoter types. These results suggest that IRF-1 promoter polymorphisms may contribute, at least partially, to host antiviral activity for chronic hepatitis C.

KW - Host immunological activity

KW - Interferon monotherapy

KW - Interferon regulatory factor

KW - Promoter polymorphims

KW - Response

UR - http://www.scopus.com/inward/record.url?scp=20444457596&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=20444457596&partnerID=8YFLogxK

U2 - 10.1016/j.hepres.2005.03.009

DO - 10.1016/j.hepres.2005.03.009

M3 - Article

C2 - 15863386

AN - SCOPUS:20444457596

VL - 32

SP - 25

EP - 32

JO - Hepatology Research

JF - Hepatology Research

SN - 1386-6346

IS - 1

ER -