PMID- 16101831
OWN - NLM
STAT- MEDLINE
DCOM- 20051228
LR  - 20201209
IS  - 0001-2815 (Print)
IS  - 0001-2815 (Linking)
VI  - 66
IP  - 3
DP  - 2005 Sep
TI  - The haplotype block, NFKBIL1-ATP6V1G2-BAT1-MICB-MICA, within the class III-class 
      I boundary region of the human major histocompatibility complex may control 
      susceptibility to hepatitis C virus-associated dilated cardiomyopathy.
PG  - 200-8
AB  - Cardiomyopathy is a heart muscle disease with impaired stretch response that can 
      result in severe heart failure and sudden death. A small proportion of hepatitis 
      C virus (HCV)-infected patients may be predisposed to develop dilated 
      cardiomyopathy (DCM) and hypertrophic cardiomyopathy (HCM). The molecular 
      mechanisms involved in the predisposition remain unknown due in part to the lack 
      of information on their genetic background. Because the human leukocyte antigen 
      (HLA) region has a pivotal role in controlling the susceptibility to HCV-induced 
      liver disease, we hypothesized that particular HLA alleles and/or non-HLA gene 
      alleles within the human major histocompatibility complex (MHC) genomic region 
      might control the predisposition to HCV-associated DCM (HCV-DCM) and/or 
      HCV-associated HCM (HCV-HCM). Here, we present mapping results of the MHC-related 
      susceptibility gene locus for HCV-associated cardiomyopathy by analyzing 
      microsatellite and single nucleotide polymorphism markers. To delineate the 
      susceptibility locus, we genotyped 44 polymorphic markers scattered across the 
      entire MHC region in a total of 59 patients (21 HCV-DCM and 38 HCV-HCM) and 120 
      controls. We mapped HCV-DCM susceptibility to a non-HLA gene locus spanning from 
      NFKBIL1 to MICA gene loci within the MHC class III-class I boundary region. Our 
      results showed that HCV-DCM was more strongly associated with alleles of the 
      non-HLA genes rather than the HLA genes themselves. In addition, no significant 
      association was found between the MHC markers and HCV-HCM. This marked difference 
      in the MHC-related disease susceptibility for HCV- associated cardiomyopathy 
      strongly suggests that the development of HCV- DCM and HCV-HCM is under the 
      control of different pathogenic mechanisms.
FAU - Shichi, D
AU  - Shichi D
AD  - Department of Basic Medical Science and Molecular Medicine, Tokai University 
      School of Medicine, Isehara, Kanagawa, Japan.
FAU - Kikkawa, E F
AU  - Kikkawa EF
FAU - Ota, M
AU  - Ota M
FAU - Katsuyama, Y
AU  - Katsuyama Y
FAU - Kimura, A
AU  - Kimura A
FAU - Matsumori, A
AU  - Matsumori A
FAU - Kulski, J K
AU  - Kulski JK
FAU - Naruse, T K
AU  - Naruse TK
FAU - Inoko, H
AU  - Inoko H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Tissue Antigens
JT  - Tissue antigens
JID - 0331072
RN  - 0 (Adaptor Proteins, Signal Transducing)
RN  - 0 (DNA Primers)
RN  - 0 (HLA Antigens)
RN  - 0 (Histocompatibility Antigens Class I)
RN  - 0 (Histocompatibility Antigens Class II)
RN  - 0 (MHC class I-related chain A)
RN  - 0 (MICB antigen)
RN  - 0 (NFKBIL1 protein, human)
RN  - EC 3.6.1.- (ATP6V1G2 protein, human)
RN  - EC 3.6.1.- (DDX39B protein, human)
RN  - EC 3.6.1.- (Vacuolar Proton-Translocating ATPases)
RN  - EC 3.6.4.13 (DEAD-box RNA Helicases)
RN  - EC 3.6.4.13 (RNA Helicases)
SB  - IM
MH  - Adaptor Proteins, Signal Transducing
MH  - Alleles
MH  - Cardiomyopathy, Dilated/*immunology/virology
MH  - Cardiomyopathy, Hypertrophic/*immunology/virology
MH  - Chromosome Mapping
MH  - DEAD-box RNA Helicases
MH  - DNA Primers/genetics
MH  - *Genetic Predisposition to Disease
MH  - Genome
MH  - Genotype
MH  - HLA Antigens/immunology
MH  - *Haplotypes
MH  - Hepacivirus/*genetics
MH  - Histocompatibility Antigens Class I/*genetics
MH  - Histocompatibility Antigens Class II
MH  - Humans
MH  - Linkage Disequilibrium
MH  - Microsatellite Repeats/genetics
MH  - Models, Genetic
MH  - Odds Ratio
MH  - Polymorphism, Single Nucleotide
MH  - Promoter Regions, Genetic
MH  - RNA Helicases/*genetics
MH  - Risk
MH  - Treatment Outcome
MH  - Vacuolar Proton-Translocating ATPases/*genetics
EDAT- 2005/08/17 09:00
MHDA- 2005/12/29 09:00
CRDT- 2005/08/17 09:00
PHST- 2005/08/17 09:00 [pubmed]
PHST- 2005/12/29 09:00 [medline]
PHST- 2005/08/17 09:00 [entrez]
AID - TAN457 [pii]
AID - 10.1111/j.1399-0039.2005.00457.x [doi]
PST - ppublish
SO  - Tissue Antigens. 2005 Sep;66(3):200-8. doi: 10.1111/j.1399-0039.2005.00457.x.