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Mamu - B*08阳性猕猴可控制猿猴免疫缺陷病毒复制。

Mamu-B*08-positive macaques control simian immunodeficiency virus replication.

作者信息

Loffredo John T, Maxwell Jess, Qi Ying, Glidden Chrystal E, Borchardt Gretta J, Soma Taeko, Bean Alex T, Beal Dominic R, Wilson Nancy A, Rehrauer William M, Lifson Jeffrey D, Carrington Mary, Watkins David I

机构信息

Wisconsin National Primate Research Center, University of Wisconsin-Madison, 555 Science Drive, Madison, WI 53711, USA.

出版信息

J Virol. 2007 Aug;81(16):8827-32. doi: 10.1128/JVI.00895-07. Epub 2007 May 30.

DOI:10.1128/JVI.00895-07
PMID:17537848
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1951344/
Abstract

Certain major histocompatibility complex (MHC) class I alleles are associated with the control of human immunodeficiency virus and simian immunodeficiency virus (SIV) replication. We have designed sequence-specific primers for detection of the rhesus macaque MHC class I allele Mamu-B08 by PCR and screened a cohort of SIV-infected macaques for this allele. Analysis of 196 SIV(mac)239-infected Indian rhesus macaques revealed that Mamu-B08 was significantly overrepresented in elite controllers; 38% of elite controllers were Mamu-B08 positive compared to 3% of progressors (P = 0.00001). Mamu-B08 was also associated with a 7.34-fold decrease in chronic phase viremia (P = 0.002). Mamu-B*08-positive macaques may, therefore, provide a good model to understand the correlates of MHC class I allele-associated immune protection and viral containment in human elite controllers.

摘要

某些主要组织相容性复合体(MHC)I类等位基因与人类免疫缺陷病毒和猿猴免疫缺陷病毒(SIV)复制的控制相关。我们设计了序列特异性引物,通过聚合酶链反应(PCR)检测恒河猴MHC I类等位基因Mamu - B08,并对一组感染SIV的猕猴进行该等位基因的筛查。对196只感染SIV(mac)239的印度恒河猴的分析显示,Mamu - B08在精英控制者中显著富集;38%的精英控制者Mamu - B08呈阳性,而疾病进展者中这一比例为3%(P = 0.00001)。Mamu - B08还与慢性期病毒血症降低7.34倍相关(P = 0.002)。因此,Mamu - B*08阳性的猕猴可能为理解人类精英控制者中MHC I类等位基因相关免疫保护和病毒控制的关联因素提供一个良好的模型。

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The antiviral efficacy of simian immunodeficiency virus-specific CD8+ T cells is unrelated to epitope specificity and is abrogated by viral escape.猿猴免疫缺陷病毒特异性CD8 + T细胞的抗病毒效力与表位特异性无关,且会因病毒逃逸而丧失。
J Virol. 2007 Mar;81(6):2624-34. doi: 10.1128/JVI.01912-06. Epub 2006 Dec 27.
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Control of simian immunodeficiency virus SIVmac239 is not predicted by inheritance of Mamu-B*17-containing haplotypes.含有Mamu - B*17单倍型的遗传并不能预测对猿猴免疫缺陷病毒SIVmac239的控制。
J Virol. 2007 Jan;81(1):406-10. doi: 10.1128/JVI.01636-06. Epub 2006 Nov 1.
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HLA Alleles Associated with Delayed Progression to AIDS Contribute Strongly to the Initial CD8(+) T Cell Response against HIV-1.与艾滋病进展延迟相关的人类白细胞抗原(HLA)等位基因对初始抗HIV-1的CD8(+) T细胞反应有很大贡献。
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Maintenance of viral suppression in HIV-1-infected HLA-B*57+ elite suppressors despite CTL escape mutations.尽管存在CTL逃逸突变,但HIV-1感染的HLA-B*57+精英抑制者仍能维持病毒抑制状态。
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6
The high-frequency major histocompatibility complex class I allele Mamu-B*17 is associated with control of simian immunodeficiency virus SIVmac239 replication.高频主要组织相容性复合体I类等位基因Mamu - B*17与猿猴免疫缺陷病毒SIVmac239复制的控制相关。
J Virol. 2006 May;80(10):5074-7. doi: 10.1128/JVI.80.10.5074-5077.2006.
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Impact of HLA-B alleles, epitope binding affinity, functional avidity, and viral coinfection on the immunodominance of virus-specific CTL responses.HLA - B等位基因、表位结合亲和力、功能亲合力及病毒合并感染对病毒特异性CTL反应免疫显性的影响。
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The high frequency Indian rhesus macaque MHC class I molecule, Mamu-B*01, does not appear to be involved in CD8+ T lymphocyte responses to SIVmac239.高频印度恒河猴MHC I类分子Mamu - B*01似乎未参与CD8 + T淋巴细胞对SIVmac239的应答。
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