PTPN22 C1858T Polymorphism and the Outcome of Hepatitis C Virus Infection

被引:5
作者
Montes-Cano, M. A. [1 ]
Garcia-Lozano, J. R. [1 ]
Aguilar-Reina, J. [2 ]
Romero-Gomez, M. [3 ]
Barroso, N. [2 ]
Nunez-Roldan, A. [1 ]
Martin, J. [4 ]
Gonzalez-Escribano, M. F. [1 ]
机构
[1] Hosp Univ Virgen del Rocio, Serv Inmunol, Seville 41013, Spain
[2] Hosp Univ Virgen del Rocio, Serv Digest, Seville 41013, Spain
[3] Hosp Univ Valme, Secc Hepatol, Serv Andaluz Salud, Seville, Spain
[4] CSIC, Inst Parasitol & Biomed Lopez Neyra, Granada, Spain
关键词
D O I
10.1089/vim.2008.0040
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The outcome of chronic hepatitis C virus infection varies, depending on viral and host factors. Those mechanisms involved in the control of the innate and adaptive response could have an influence on the outcome of infection. The PTPN22 gene encodes an intracellular lymphoid-specific phosphatase (Lyp) with a lymphocyte activating downregulatory effect. A single-nucleotide polymorphism (SNP) C1858T located on this gene has been associated with autoimmune diseases and bacterial infections. The aim of this study was to assess whether the PTPN22 C1858T polymorphism is related to the outcome of hepatitis C viral infection. A total of 69 patients with spontaneous viral clearance (SVC), 281 patients with chronic hepatitis C (CHC), and 1036 individuals not infected with hepatitis C (NIC) were included in this study. Patients with CHC were stratified according to Scheuer score of hepatic fibrosis from F0-F2 (n = 200) and F3-F4 (n = 81), and according to their response to therapy in patients with sustained responses (SR; n = 103) and non-sustained response (NSR; n = 104). Genotyping of the C1858T polymorphism was performed using TaqMan probes. No statistically significant differences in the distribution of PTPN22 C1858T polymorphism were observed upon comparison of patient group with the NIC group. Also, when the different patient groups were compared to one another, no statistically significant differences were detected: the SVC with the CHC group (10.2% versus 12.5%; p = 0.6), the F0-F2 with the F3-F4 group (11.5% versus 14.8%; p = 0.5), and the NSR with the SR group (11.5% versus 14.6%; p = 0.4). Our results do not support a major role of this polymorphism of the PTPN22 gene in the outcome of chronic hepatitis C virus infection in the Spanish population.
引用
收藏
页码:491 / 494
页数:4
相关论文
共 22 条
  • [1] Protein tyrosine phosphatases in the human genome
    Alonso, A
    Sasin, J
    Bottini, N
    Friedberg, I
    Friedberg, I
    Osterman, A
    Godzik, A
    Hunter, T
    Dixon, J
    Mustelin, T
    [J]. CELL, 2004, 117 (06) : 699 - 711
  • [2] EPIDEMIOLOGY OF HEPATITIS-C IN THE WEST
    ALTER, MJ
    [J]. SEMINARS IN LIVER DISEASE, 1995, 15 (01) : 5 - 14
  • [3] A genomic perspective on protein tyrosine phosphatases: gene structure, pseudogenes, and genetic disease linkage
    Andersen, JN
    Jansen, PG
    Echwald, SM
    Mortensen, OH
    Fukada, T
    Del Vecchio, R
    Tonks, NK
    Moller, NPH
    [J]. FASEB JOURNAL, 2004, 18 (01) : 8 - 30
  • [4] A missense single-nucleotide polymorphism in a gene encoding a protein tyrosine phosphatase (PTPN22) is associated with rheumatoid arthritis
    Begovich, AB
    Carlton, VEH
    Honigberg, LA
    Schrodi, SJ
    Chokkalingam, AP
    Alexander, HC
    Ardlie, KG
    Huang, QQ
    Smith, AM
    Spoerke, JM
    Conn, MT
    Chang, M
    Chang, SYP
    Saiki, RK
    Catanese, JJ
    Leong, DU
    Garcia, VE
    McAllister, LB
    Jeffery, DA
    Lee, AT
    Batliwalla, F
    Remmers, E
    Criswell, LA
    Seldin, MF
    Kastner, DL
    Amos, CI
    Sninsky, JJ
    Gregersen, PK
    [J]. AMERICAN JOURNAL OF HUMAN GENETICS, 2004, 75 (02) : 330 - 337
  • [5] A functional variant of lymphoid tyrosine phosphatase is associated with type I diabetes
    Bottini, N
    Musumeci, L
    Alonso, A
    Rahmouni, S
    Nika, K
    Rostamkhani, M
    MacMurray, J
    Meloni, GF
    Lucarelli, P
    Pellecchia, M
    Eisenbarth, GS
    Comings, D
    Mustelin, T
    [J]. NATURE GENETICS, 2004, 36 (04) : 337 - 338
  • [6] PTPN22 and invasive bacterial disease
    Chapman, SJ
    Khor, CC
    O Vannberg, F
    Maskell, NA
    Davies, CW
    Hedley, EL
    Segal, S
    Moore, CE
    Knox, K
    Day, NP
    Gillespie, SH
    Crook, DW
    Davies, RJ
    Hill, AV
    [J]. NATURE GENETICS, 2006, 38 (05) : 499 - 500
  • [7] PTPN22:: Its role in SLE and autoimmunity
    Chung, Sharon A.
    Criswell, Lindsey A.
    [J]. AUTOIMMUNITY, 2007, 40 (08) : 582 - 590
  • [8] Cloning and characterization of a lymphoid-specific, inducible human protein tyrosine phosphatase, Lyp
    Cohen, S
    Dadi, H
    Shaoul, E
    Sharfe, N
    Roifman, CM
    [J]. BLOOD, 1999, 93 (06) : 2013 - 2024
  • [9] Analysis of families in the multiple autoimmune disease genetics consortium (MADGC) collection:: the PTPN22 620W allele associates with multiple autoimmune phenotypes
    Criswell, LA
    Pfeiffer, KA
    Lum, RF
    Gonzales, B
    Novitzke, J
    Moser, KL
    Begovich, AB
    Carlton, VEH
    Li, W
    Lee, AT
    Ortmann, W
    Behrens, TW
    Gregersen, PK
    [J]. AMERICAN JOURNAL OF HUMAN GENETICS, 2005, 76 (04) : 561 - 571
  • [10] POSSIBLE MECHANISM INVOLVING T-LYMPHOCYTE RESPONSE TO NONSTRUCTURAL PROTEIN-3 IN VIRAL CLEARANCE IN ACUTE HEPATITIS-C VIRUS-INFECTION
    DIEPOLDER, HM
    ZACHOVAL, R
    HOFFMANN, RM
    WIERENGA, EA
    SANTANTONIO, T
    JUNG, MC
    EICHENLAUB, D
    PAPE, GR
    [J]. LANCET, 1995, 346 (8981): : 1006 - 1007