在慢性1型人类免疫缺陷病毒感染中，补偿性突变部分恢复了适应性，并延缓了免疫显性的HLA-B*5703限制性Gag表位内逃逸突变的回复。
Compensatory mutation partially restores fitness and delays reversion of escape mutation within the immunodominant HLA-B*5703-restricted Gag epitope in chronic human immunodeficiency virus type 1 infection.
作者信息
Crawford Hayley, Prado Julia G, Leslie Alasdair, Hué Stéphane, Honeyborne Isobella, Reddy Sharon, van der Stok Mary, Mncube Zenele, Brander Christian, Rousseau Christine, Mullins James I, Kaslow Richard, Goepfert Paul, Allen Susan, Hunter Eric, Mulenga Joseph, Kiepiela Photini, Walker Bruce D, Goulder Philip J R
机构信息
Department of Pediatrics, University of Oxford, Peter Medawar Building for Pathogen Research, South Parks Rd., Oxford OX1 3SY, United Kingdom.
出版信息
J Virol. 2007 Aug;81(15):8346-51. doi: 10.1128/JVI.00465-07. Epub 2007 May 16.
Abstract
HLA-B5703 is associated with effective immune control in human immunodeficiency virus type 1 (HIV-1) infection. Here we describe an escape mutation within the immunodominant HLA-B5703-restricted epitope in chronic HIV-1 infection, KAFSPEVIPMF (Gag 162-172), and demonstrate that this mutation reduces viral replicative capacity. Reversion of this mutation following transmission to HLA-B5703-negative recipients was delayed by the compensatory mutation S165N within the same epitope. These data may help explain the observed association between HLA-B5703 and long-term control of viremia.
摘要
HLA - B5703与1型人类免疫缺陷病毒（HIV - 1）感染中的有效免疫控制相关。在此，我们描述了慢性HIV - 1感染中免疫显性的HLA - B5703限制性表位KAFSPEVIPMF（Gag 162 - 172）内的一个逃逸突变，并证明该突变降低了病毒复制能力。在传播给HLA - B5703阴性受者后，同一表位内的补偿性突变S165N延迟了该突变的回复。这些数据可能有助于解释观察到的HLA - B5703与病毒血症长期控制之间的关联。
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本文引用的文献
1
High rates of forward transmission events after acute/early HIV-1 infection.
J Infect Dis. 2007 Apr 1;195(7):951-9. doi: 10.1086/512088. Epub 2007 Feb 16.
2
Vaccine-induced T cells control reversion of AIDS virus immune escape mutants.
J Virol. 2007 Apr;81(8):4137-44. doi: 10.1128/JVI.02193-06. Epub 2007 Jan 24.
3
Control of human immunodeficiency virus type 1 is associated with HLA-B*13 and targeting of multiple gag-specific CD8+ T-cell epitopes.
J Virol. 2007 Apr;81(7):3667-72. doi: 10.1128/JVI.02689-06. Epub 2007 Jan 24.
4
CD8 T-cell recognition of multiple epitopes within specific Gag regions is associated with maintenance of a low steady-state viremia in human immunodeficiency virus type 1-seropositive patients.
J Virol. 2007 Mar;81(5):2440-8. doi: 10.1128/JVI.01847-06. Epub 2006 Dec 20.
5
CD8+ T-cell responses to different HIV proteins have discordant associations with viral load.
Nat Med. 2007 Jan;13(1):46-53. doi: 10.1038/nm1520. Epub 2006 Dec 17.
6
Mutually exclusive T-cell receptor induction and differential susceptibility to human immunodeficiency virus type 1 mutational escape associated with a two-amino-acid difference between HLA class I subtypes.
J Virol. 2007 Feb;81(4):1619-31. doi: 10.1128/JVI.01580-06. Epub 2006 Nov 22.
7
Rapid reversion of sequence polymorphisms dominates early human immunodeficiency virus type 1 evolution.
J Virol. 2007 Jan;81(1):193-201. doi: 10.1128/JVI.01231-06. Epub 2006 Oct 25.
8
Human leukocyte antigen B58 supertype and human immunodeficiency virus type 1 infection in native Africans.
J Virol. 2006 Jun;80(12):6056-60. doi: 10.1128/JVI.02119-05.
9
Use of a novel assay based on intact recombinant viruses expressing green (EGFP) or red (DsRed2) fluorescent proteins to examine the contribution of pol and env genes to overall HIV-1 replicative fitness.
J Virol Methods. 2006 Sep;136(1-2):102-17. doi: 10.1016/j.jviromet.2006.04.004. Epub 2006 May 11.
10
Fitness cost of escape mutations in p24 Gag in association with control of human immunodeficiency virus type 1.
J Virol. 2006 Apr;80(7):3617-23. doi: 10.1128/JVI.80.7.3617-3623.2006.
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