PMID- 12225333
OWN - NLM
STAT- MEDLINE
DCOM- 20021204
LR  - 20191106
IS  - 1352-0504 (Print)
IS  - 1352-0504 (Linking)
VI  - 9
IP  - 5
DP  - 2002 Sep
TI  - A single nucleotide polymorphism of the low molecular mass polypeptide 7 gene 
      influences the interferon response in patients with chronic hepatitis C.
PG  - 377-84
AB  - Transporter associated with antigen processing (TAP) and low molecular mass 
      polypeptides (LMP) play crucial roles in the human leukocyte antigen (HLA) class 
      I-restricted antigen presenting systems. This study was performed to elucidate 
      whether these antigen-presenting gene polymorphisms could influence the response 
      to interferon (IFN) treatment in patients with chronic hepatitis C. Polymorphisms 
      of TAP and LMP genes in 175 hepatitis C virus (HCV) patients were determined by 
      polymerase chain reaction-restriction fragment length polymorphism. The 
      frequencies of these genes were compared between sustained-responders (n=49) and 
      nonresponders (n=126), classified by biochemical and virological responses to 
      IFN. The distributions of TAP1*, TAP2*, and LMP2 genes between 
      sustained-responders and nonresponders did not differ. However, LMP7-K gene 
      frequency in sustained-responders was higher than that in nonresponders [odds 
      ratio 2.3 (95% confidence interval 1.1-4.6); 16%vs 7.9%]. Multivariate analysis 
      revealed that LMP7-K and HCV-RNA quantity were independent factors influencing 
      the outcome of IFN therapy [4.5 (1.4-14); P=0.011, 0.40 (0.24-0.65); P=0.0003, 
      respectively]. Furthermore, among patients with a low viral load (< or = 2.0 
      Meq/mL), the LMP7-K positive patients had an even higher ratio of sustained 
      response compared to those without LMP7-K [5.9 (1.6-22); 82%vs 44%; P=0.0062]. 
      These findings suggest that a single nucleotide polymorphism of LMP7 gene is one 
      of the important host factors which independently influence the response to IFN 
      in patients with chronic hepatitis C.
FAU - Sugimoto, Y
AU  - Sugimoto Y
AD  - Department of Molecular Therapeutics, Osaka University Graduate School of 
      Medicine, Suita, Osaka, Japan.
FAU - Kuzushita, N
AU  - Kuzushita N
FAU - Takehara, T
AU  - Takehara T
FAU - Kanto, T
AU  - Kanto T
FAU - Tatsumi, T
AU  - Tatsumi T
FAU - Miyagi, T
AU  - Miyagi T
FAU - Jinushi, M
AU  - Jinushi M
FAU - Ohkawa, K
AU  - Ohkawa K
FAU - Horimoto, M
AU  - Horimoto M
FAU - Kasahara, A
AU  - Kasahara A
FAU - Hori, M
AU  - Hori M
FAU - Sasaki, Y
AU  - Sasaki Y
FAU - Hayashi, N
AU  - Hayashi N
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - J Viral Hepat
JT  - Journal of viral hepatitis
JID - 9435672
RN  - 0 (ATP Binding Cassette Transporter, Subfamily B, Member 3)
RN  - 0 (ATP-Binding Cassette Transporters)
RN  - 0 (Integration Host Factors)
RN  - 0 (Interferon-alpha)
RN  - 0 (Multienzyme Complexes)
RN  - 145892-13-3 (TAP2 protein, human)
RN  - EC 3.4.22.- (Cysteine Endopeptidases)
RN  - EC 3.4.25.1 (LMP7 protein)
RN  - EC 3.4.25.1 (Proteasome Endopeptidase Complex)
SB  - IM
MH  - ATP Binding Cassette Transporter, Subfamily B, Member 3
MH  - ATP-Binding Cassette Transporters/genetics
MH  - Adult
MH  - Cysteine Endopeptidases/*genetics
MH  - Female
MH  - Gene Frequency
MH  - Genotype
MH  - Hepatitis C, Chronic/drug therapy/*genetics/virology
MH  - Humans
MH  - Integration Host Factors
MH  - Interferon-alpha/*therapeutic use
MH  - Male
MH  - *Multienzyme Complexes
MH  - Multivariate Analysis
MH  - Polymerase Chain Reaction
MH  - *Polymorphism, Single Nucleotide
MH  - Proteasome Endopeptidase Complex
MH  - Treatment Outcome
MH  - Viral Load
EDAT- 2002/09/13 10:00
MHDA- 2002/12/05 04:00
CRDT- 2002/09/13 10:00
PHST- 2002/09/13 10:00 [pubmed]
PHST- 2002/12/05 04:00 [medline]
PHST- 2002/09/13 10:00 [entrez]
AID - 365 [pii]
AID - 10.1046/j.1365-2893.2002.00365.x [doi]
PST - ppublish
SO  - J Viral Hepat. 2002 Sep;9(5):377-84. doi: 10.1046/j.1365-2893.2002.00365.x.