PMID- 24059286
OWN - NLM
STAT- MEDLINE
DCOM- 20140623
LR  - 20211021
IS  - 1471-2334 (Electronic)
IS  - 1471-2334 (Linking)
VI  - 13
DP  - 2013 Sep 2
TI  - KIR3DS1/L1 and HLA-Bw4-80I are associated with HIV disease progression among HIV 
      typical progressors and long-term nonprogressors.
PG  - 405
LID - 10.1186/1471-2334-13-405 [doi]
AB  - BACKGROUND: Natural killer (NK) cells have emerged as pivotal players in innate 
      immunity, especially in the defense against viral infections and tumors. Killer 
      immunoglobulin-like receptors (KIRs)--an important recognition receptor expressed 
      on the surface of NK cells--regulate the inhibition and/or activation of NK cells 
      after interacting with human leukocyte antigen (HLA) class I ligands. Various KIR 
      genes might impact the prognosis of many different diseases. The implications of 
      KIR-HLA interaction in HIV disease progression remains poorly understood. 
      METHODS: Here, we studied KIR genotypes, mRNA levels, HLA genotypes, CD4+ T cell 
      counts and viral loads in our cohort of Human Immunodeficiency Virus 
      (HIV)-infected individuals, a group that includes HIV long-term nonprogressors 
      (LTNPs) and typical progressors (TPs). RESULTS: We found that the frequency of 
      KIR3DS1/L1 heterozygotes with HLA-Bw4-80I gene was much higher in LTNPs than in 
      TPs (P = 0.001) and that the KIR3DL1 homozygotes without HLA-Bw4-80I gene had 
      higher viral loads and lower CD4+ T cell counts (P = 0.014 and P = 0.021, 
      respectively). Our study also confirmed that homozygosity for the HLA-Bw6 allele 
      was associated with rapid disease progression. In addition to the aforementioned 
      results on the DNA level, we observed that higher level expression of KIR3DS1 
      mRNA was in LTNP group, and that higher level expression of KIR3DL1 mRNA was in 
      TP group. CONCLUSIONS: Our data suggest that different KIR-HLA genotypes and 
      different levels of transcripts associate with HIV disease progression.
FAU - Jiang, Yongjun
AU  - Jiang Y
AD  - Key Laboratory of AIDS Immunology of Ministry of Health, Department of Laboratory 
      Medicine, The First Affiliated Hospital, China Medical University, Shenyang 
      110001, P, R, China. hongshang100@hotmail.com.
FAU - Chen, Ou
AU  - Chen O
FAU - Cui, Chen
AU  - Cui C
FAU - Zhao, Bin
AU  - Zhao B
FAU - Han, Xiaoxu
AU  - Han X
FAU - Zhang, Zining
AU  - Zhang Z
FAU - Liu, Jing
AU  - Liu J
FAU - Xu, Junjie
AU  - Xu J
FAU - Hu, Qinghai
AU  - Hu Q
FAU - Liao, Christina
AU  - Liao C
FAU - Shang, Hong
AU  - Shang H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130902
PL  - England
TA  - BMC Infect Dis
JT  - BMC infectious diseases
JID - 100968551
RN  - 0 (HLA-B Antigens)
RN  - 0 (HLA-Bw4 antigen)
RN  - 0 (Receptors, KIR3DL1)
RN  - 0 (Receptors, KIR3DS1)
SB  - IM
MH  - Alleles
MH  - CD4 Lymphocyte Count
MH  - CD4-Positive T-Lymphocytes/cytology
MH  - Disease Progression
MH  - Genotype
MH  - HIV Infections/blood/*genetics/metabolism/virology
MH  - HLA-B Antigens/*genetics/metabolism
MH  - Humans
MH  - Receptors, KIR3DL1/*genetics/metabolism
MH  - Receptors, KIR3DS1/*genetics/metabolism
PMC - PMC3766012
EDAT- 2013/09/26 06:00
MHDA- 2014/06/24 06:00
PMCR- 2013/09/02
CRDT- 2013/09/25 06:00
PHST- 2013/04/12 00:00 [received]
PHST- 2013/08/30 00:00 [accepted]
PHST- 2013/09/25 06:00 [entrez]
PHST- 2013/09/26 06:00 [pubmed]
PHST- 2014/06/24 06:00 [medline]
PHST- 2013/09/02 00:00 [pmc-release]
AID - 1471-2334-13-405 [pii]
AID - 10.1186/1471-2334-13-405 [doi]
PST - epublish
SO  - BMC Infect Dis. 2013 Sep 2;13:405. doi: 10.1186/1471-2334-13-405.