PMID- 29280757
OWN - NLM
STAT- MEDLINE
DCOM- 20190919
LR  - 20190919
IS  - 1473-5571 (Electronic)
IS  - 0269-9370 (Linking)
VI  - 32
IP  - 7
DP  - 2018 Apr 24
TI  - KIR3DL1 alleles and their epistatic interactions with human leukocyte antigen 
      class I influence resistance and susceptibility to HIV-1 acquisition in the 
      Pumwani sex worker cohort.
PG  - 841-850
LID - 10.1097/QAD.0000000000001735 [doi]
AB  - OBJECTIVE: To determine the associations of KIR3DL1/S1(3DL1/S1) and its epistatic 
      interactions with human leukocyte antigen class I (HLA-I) alleles with resistance 
      and susceptibility to HIV-1. DESIGN: Despite repeated exposure to HIV-1, a subset 
      of women enrolled in the Pumwani sex worker cohort remain HIV uninfected. 
      Previous studies have shown that specific HLA class I and II alleles were 
      associated with this natural immunity. In this study, we investigated the 
      association of 3DL1/S1 and its epistatic interactions with HLA-I, with resistance 
      or susceptibility to HIV-1 acquisition. METHODS: We used a sequence-based typing 
      method to genotype 3DL1/S1 of 641 women in this cohort. The association of 
      3DL1/S1 and its epistatic interactions with HLA-I were analyzed using SPSS 
      statistics software. RESULTS: 3DL1041 is enriched in the HIV-1-resistant women 
      [P = 0.009, Pc = 0.0468, odds ratio (OR): 3.359, 95% confidence interval (CI): 
      1.39-8.32], whereas, 3DL1020 was associated with susceptibility to HIV-1 
      infection before correction for multiple comparisons (P = 0.029, Pc = 0.0858, OR: 
      0.316, 95%CI: 0.10-1.04). Epistatic interactions between several 3DL1 alleles and 
      specific HLA-I alleles were observed. Among them the cocarriage of 3DL1041 with 
      Bw4 (P = 1E - 05, Pc = 0.0015, OR: 13.33, 95%CI: 3.43-51.9), or Bw6 (P = 0.008, 
      Pc = 0.272, OR: 3.92, 95%CI: 1.51-10.17), increased the odds of remaining HIV-1 
      uninfected. Further, 3DL1041+/Bw4+ women who entered the cohort HIV negative 
      remained uninfected (P = 0.032, Pc = 0.0858). Cocarriage of 3DL101501 with 
      C02 : 10 (P = 2.73E - 07, Pc = 7.0954E - 06), B15 : 03 (P = 3.21E - 04, 
      Pc = 0.0042), A24 supertype (P = 8.89E - 04, Pc = 0.0077), or A23 : 01 
      (P = 0.0036, Pc = 0.0236) was associated with increased susceptibility to 
      seroconversion. CONCLUSION: The effects of interactions between 3DL1 and HLA-I 
      alleles on resistance/susceptibility to HIV-1 infection suggest that innate 
      immunity plays an important role in HIV-1 acquisition and should be studied and 
      explored for HIV prevention.
FAU - Luo, Ma
AU  - Luo M
AD  - HIV and Host Genetics, National Microbiology Laboratory, Public Health Agency of 
      Canada.
AD  - Department of Medical Microbiology, University of Manitoba, Winnipeg, Manitoba, 
      Canada.
FAU - Czarnecki, Chris
AU  - Czarnecki C
AD  - HIV and Host Genetics, National Microbiology Laboratory, Public Health Agency of 
      Canada.
FAU - Nebroski, Michelle
AU  - Nebroski M
AD  - HIV and Host Genetics, National Microbiology Laboratory, Public Health Agency of 
      Canada.
FAU - Kimani, Joshua
AU  - Kimani J
AD  - Department of Medical Microbiology, University of Manitoba, Winnipeg, Manitoba, 
      Canada.
AD  - Department of Medical Microbiology, University of Nairobi, Nairobi, Kenya.
FAU - Bernard, Nicole
AU  - Bernard N
AD  - Division of Experimental Medicine and the Infectious Disease, Research Institute 
      of the McGill University Health Centre, McGill University, Montreal, Quebec, 
      Canada.
FAU - Plummer, Francis A
AU  - Plummer FA
AD  - HIV and Host Genetics, National Microbiology Laboratory, Public Health Agency of 
      Canada.
AD  - Department of Medical Microbiology, University of Manitoba, Winnipeg, Manitoba, 
      Canada.
LA  - eng
GR  - Canadian Institutes of Health Research/International
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - AIDS
JT  - AIDS (London, England)
JID - 8710219
RN  - 0 (Histocompatibility Antigens Class I)
RN  - 0 (KIR3DL1 protein, human)
RN  - 0 (KIR3DS1 protein, human)
RN  - 0 (Receptors, KIR3DL1)
RN  - 0 (Receptors, KIR3DS1)
SB  - IM
MH  - Alleles
MH  - Cohort Studies
MH  - *Disease Susceptibility
MH  - *Epistasis, Genetic
MH  - Female
MH  - Follow-Up Studies
MH  - Genotype
MH  - Genotyping Techniques
MH  - HIV Infections/*genetics
MH  - Histocompatibility Antigens Class I/*genetics/metabolism
MH  - Humans
MH  - Immunity, Innate
MH  - Kenya
MH  - Receptors, KIR3DL1/*genetics/metabolism
MH  - Receptors, KIR3DS1/genetics/metabolism
MH  - Sequence Analysis, DNA
MH  - *Sex Workers
EDAT- 2017/12/28 06:00
MHDA- 2019/09/20 06:00
CRDT- 2017/12/28 06:00
PHST- 2017/12/28 06:00 [pubmed]
PHST- 2019/09/20 06:00 [medline]
PHST- 2017/12/28 06:00 [entrez]
AID - 10.1097/QAD.0000000000001735 [doi]
PST - ppublish
SO  - AIDS. 2018 Apr 24;32(7):841-850. doi: 10.1097/QAD.0000000000001735.