PMID- 25119688
OWN - NLM
STAT- MEDLINE
DCOM- 20150226
LR  - 20220321
IS  - 1473-5571 (Electronic)
IS  - 0269-9370 (Linking)
VI  - 27
IP  - 18
DP  - 2013 Nov 28
TI  - On stand by: host genetics of HIV control.
PG  - 2831-9
LID - 10.1097/01.aids.0000432536.85335.c8 [doi]
AB  - The impact of host genetic variation on determining the differential outcomes 
      after HIV infection has been studied by two approaches: targeting of candidate 
      genes and genome-wide association studies (GWASs). The overlap in genetic 
      variants that has been identified by these two means has essentially been 
      restricted to variants near to the human leukocyte antigen (HLA) class I genes, 
      although variation in the CCR5 locus, which was first shown to have an effect on 
      HIV outcomes using the candidate gene approach, does reach significance 
      genome-wide when very large samples sizes (i.e. thousands) are used in GWAS. 
      Overall, many of the variants identified by the candidate gene approach are 
      likely to be spurious, as no additional variants apart from a novel variant near 
      the HLA-C gene have been consistently identified by GWAS. Variants with low 
      frequency and/or low impact on HIV outcomes are likely to exist in the genome and 
      there could be many of them, but these are not identifiable, given current GWAS 
      sample sizes. Several loci centrally involved in the immune response, including 
      the immunoglobulin genes, T-cell receptor loci, or leukocyte receptor complex, 
      are either poorly covered on the GWAS chips or difficult to interpret due to 
      their repetitive nature and/or the presence of insertion/deletion polymorphisms 
      in the region. These loci warrant further interrogation, but genetic 
      characterization of these regions across a range of individuals will first be 
      required. Finally, synergistic interactions between loci may affect outcome after 
      infection, as suggested by associations of specific, functionally relevant HLA 
      and killer cell immunoglobulin-like receptor variants with HIV disease outcomes, 
      and these require further consideration as well.
FAU - Carrington, Mary
AU  - Carrington M
AD  - aCancer and Inflammation Program, Laboratory of Experimental Immunology, SAIC 
      Frederick Inc., Frederick National Laboratory for Cancer Research, Frederick, 
      Maryland bRagon Institute of MGH, MIT and Harvard, Boston, Massachusetts, USA 
      cSchool of Life Sciences, Ecole Polytechnique Federale de Lausanne dInstitute of 
      Microbiology, University Hospital Center and University of Lausanne, Lausanne, 
      Switzerland eProgram in Medical and Population Genetics, Broad Institute of MIT 
      and Harvard, Cambridge, Massachusetts, USA.
FAU - Bashirova, Arman A
AU  - Bashirova AA
FAU - McLaren, Paul J
AU  - McLaren PJ
LA  - eng
GR  - HHSN261200800001E/PHS HHS/United States
GR  - Intramural NIH HHS/United States
PT  - Editorial
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, N.I.H., Intramural
PT  - Review
PL  - England
TA  - AIDS
JT  - AIDS (London, England)
JID - 8710219
SB  - IM
MH  - Biomedical Research/trends
MH  - *Genetics, Medical
MH  - Genome-Wide Association Study
MH  - HIV Infections/*genetics/*immunology
MH  - Humans
MH  - *Immunogenetics
EDAT- 2014/08/15 06:00
MHDA- 2015/02/27 06:00
CRDT- 2014/08/15 06:00
PHST- 2014/08/15 06:00 [entrez]
PHST- 2014/08/15 06:00 [pubmed]
PHST- 2015/02/27 06:00 [medline]
AID - 00002030-201311280-00002 [pii]
AID - 10.1097/01.aids.0000432536.85335.c8 [doi]
PST - ppublish
SO  - AIDS. 2013 Nov 28;27(18):2831-9. doi: 10.1097/01.aids.0000432536.85335.c8.