PMID- 19775370
OWN - NLM
STAT- MEDLINE
DCOM- 20091222
LR  - 20111117
IS  - 1399-0039 (Electronic)
IS  - 0001-2815 (Linking)
VI  - 74
IP  - 4
DP  - 2009 Oct
TI  - HLA-G polymorphism influences the susceptibility to HCV infection in sickle cell 
      disease patients.
PG  - 308-13
LID - 10.1111/j.1399-0039.2009.01331.x [doi]
AB  - Despite its well known monogenic etiopathogenesis, sickle cell disease (SCD) is 
      characterized by a striking variability of clinical presentation. There is 
      growing evidence that genetic factors may be involved in this variability. Human 
      leukocyte antigen (HLA)-G is a non-classical HLA molecule which was shown to be 
      expressed at sites of inflammation and in inflammatory diseases. Besides its 
      large and highly polymorphic promoter region, the 3' UTR region seems also to 
      play an important role on regulating HLA-G expression. We investigated the 
      influence of the 14 pb (rs1704) and the +3142 (rs1063320) HLA-G polymorphisms in 
      93 SCD patients in order to evaluate its potential role on clinical parameters. 
      Twenty-one patients presented an HCV infection. Among all SCD patients 16 (22.2%) 
      were homozygous for the +3142C genotype, none of them hepatitis C (HCV) positive. 
      Controlling for blood transfusions in the last year, the C allele represented a 
      dose dependent protection effect for HCV infection (PR = 0.41; 95% CI: 
      0.24-0.71). The +3142C allele was also underrepresented among patients with 
      history of respiratory-tract infections. Our results support a role of the +3142 
      polymorphism in the susceptibility to infections, in particular to HCV infection, 
      and suggest a possible interference of the HLA-G molecule in the response to 
      infections, among SCD patients.
FAU - Cordero, E A A
AU  - Cordero EA
AD  - Post-Graduation Program in Medical Sciences, Hospital de Clinicas de Porto Alegre 
      (HCPA), Porto Alegre, Brazil.
FAU - Veit, T D
AU  - Veit TD
FAU - da Silva, M A L
AU  - da Silva MA
FAU - Jacques, S M C
AU  - Jacques SM
FAU - Silla, L M D R
AU  - Silla LM
FAU - Chies, J A B
AU  - Chies JA
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Tissue Antigens
JT  - Tissue antigens
JID - 0331072
RN  - 0 (HLA Antigens)
RN  - 0 (HLA-G Antigens)
RN  - 0 (Histocompatibility Antigens Class I)
SB  - IM
EIN - Tissue Antigens. 2009 Nov;74(5):465
CIN - Tissue Antigens. 2010 Mar;75(3):199-200. PMID: 20030785
MH  - Adult
MH  - Anemia, Sickle Cell/*genetics/immunology/*virology
MH  - Case-Control Studies
MH  - Disease Susceptibility
MH  - Female
MH  - HLA Antigens/*genetics
MH  - HLA-G Antigens
MH  - Hepacivirus/*genetics
MH  - Hepatitis C/complications/*genetics/immunology
MH  - Histocompatibility Antigens Class I/*genetics
MH  - Humans
MH  - Male
MH  - Polymorphism, Genetic/*genetics
MH  - Young Adult
EDAT- 2009/09/25 06:00
MHDA- 2009/12/23 06:00
CRDT- 2009/09/25 06:00
PHST- 2009/09/25 06:00 [entrez]
PHST- 2009/09/25 06:00 [pubmed]
PHST- 2009/12/23 06:00 [medline]
AID - TAN1331 [pii]
AID - 10.1111/j.1399-0039.2009.01331.x [doi]
PST - ppublish
SO  - Tissue Antigens. 2009 Oct;74(4):308-13. doi: 10.1111/j.1399-0039.2009.01331.x.