PMID- 9864033
OWN - NLM
STAT- MEDLINE
DCOM- 19990317
LR  - 20190826
IS  - 0001-2815 (Print)
IS  - 0001-2815 (Linking)
VI  - 52
IP  - 5
DP  - 1998 Nov
TI  - Donor-recipient sharing of HLA class II alleles predicts earlier recurrence and 
      accelerated progression of hepatitis C following liver transplantation.
PG  - 435-43
AB  - Both direct viral cytopathic effects and host immune responses appear to be 
      important in the pathogenesis of hepatitis C virus (HCV) infection. Liver 
      transplantation provides a means to explore the role of the immune system in the 
      development of HCV-related liver damage through comparing the natural history of 
      HCV in patients with different degrees of donor-recipient human leukocyte antigen 
      (HLA) matching. We evaluated 36 patients with recurrent hepatitis C viremia 
      following liver transplantation to determine whether hepatocellular injury or 
      progression to bridging fibrosis occur more rapidly when donor and recipients 
      share HLA alleles. HLA typing for the HLA-A and HLA-B loci was performed by 
      serological techniques and PCR-based oligotyping was used to type alleles of the 
      DRB1, DRB3, DQA1, and DQB1 loci. A median of eight liver biopsies, obtained 
      during a median follow-up of 36 months, were reviewed per patient. 
      Donor-recipient sharing of alleles of HLA-DQB1 or DRB1 was associated with more 
      rapid development of recurrent hepatitis by univariate analysis (chi2=5.7, P=0.02 
      and chi2=5.54, P=0.02 respectively). However, only sharing of HLA-DRB1 alleles 
      was identified as an independent predictor of reduced time to recurrent 
      histologic injury by multivariate analysis (chi2 =5.74, P=0.02). Furthermore, 
      sharing of HLA-DRB3 and histologic evidence of rejection were associated with 
      more rapid progression to bridging fibrosis both by univariate methods 
      (chi2=4.12, P=0.04 and chi2=4.66, P=0.03 respectively), and by multivariate 
      analysis (chi2=13.01, P=0.001). These findings suggest that HLA class 
      II-restricted immune responses may contribute to the pathogenesis of HCV-related 
      liver injury in liver transplant recipients.
FAU - Cotler, S J
AU  - Cotler SJ
AD  - Department of Medicine, University of Washington Medical Center, Seattle, USA.
FAU - Gaur, L K
AU  - Gaur LK
FAU - Gretch, D R
AU  - Gretch DR
FAU - Wile, M
AU  - Wile M
FAU - Strong, D M
AU  - Strong DM
FAU - Bronner, M P
AU  - Bronner MP
FAU - Carithers, R L Jr
AU  - Carithers RL Jr
FAU - Emond, M J
AU  - Emond MJ
FAU - Perkins, J D
AU  - Perkins JD
FAU - Nelson, K A
AU  - Nelson KA
LA  - eng
PT  - Journal Article
PL  - England
TA  - Tissue Antigens
JT  - Tissue antigens
JID - 0331072
RN  - 0 (Histocompatibility Antigens Class II)
RN  - 0 (RNA, Viral)
SB  - IM
MH  - Adult
MH  - *Alleles
MH  - Disease Progression
MH  - Female
MH  - Hepatitis C, Chronic/genetics/*immunology
MH  - Histocompatibility
MH  - Histocompatibility Antigens Class II/*genetics/*immunology
MH  - Humans
MH  - Liver Transplantation/adverse effects/*immunology
MH  - Male
MH  - Middle Aged
MH  - RNA, Viral/blood
MH  - Recurrence
MH  - Time Factors
EDAT- 1998/12/24 03:03
MHDA- 2001/03/28 10:01
CRDT- 1998/12/24 03:03
PHST- 1998/12/24 03:03 [pubmed]
PHST- 2001/03/28 10:01 [medline]
PHST- 1998/12/24 03:03 [entrez]
AID - 10.1111/j.1399-0039.1998.tb03070.x [doi]
PST - ppublish
SO  - Tissue Antigens. 1998 Nov;52(5):435-43. doi: 10.1111/j.1399-0039.1998.tb03070.x.