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婴儿1型人类免疫缺陷病毒感染中细胞毒性T淋巴细胞逃逸突变体的独特获得情况。

Unique acquisition of cytotoxic T-lymphocyte escape mutants in infant human immunodeficiency virus type 1 infection.

作者信息

Pillay Thillagavathie, Zhang Hua-Tang, Drijfhout Jan W, Robinson Nicola, Brown Helen, Khan Munira, Moodley Jagadesa, Adhikari Miriam, Pfafferott Katja, Feeney Margaret E, St John Anne, Holmes Edward C, Coovadia Hoosen M, Klenerman Paul, Goulder Philip J R, Phillips Rodney E

机构信息

The Peter Medawar Building for Pathogen Research and Nuffield Department of Medicine, John Radcliffe Hospital, Oxford, United Kingdom.

出版信息

J Virol. 2005 Sep;79(18):12100-5. doi: 10.1128/JVI.79.18.12100-12105.2005.

DOI:10.1128/JVI.79.18.12100-12105.2005
PMID:16140787
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1212591/
Abstract

The role of cytotoxic T-lymphocyte (CTL) escape in rapidly progressive infant human immunodeficiency virus type 1 (HIV-1) infection is undefined. The data presented here demonstrate that infant HIV-1-specific CTL can select for viral escape variants very early in life. These variants, furthermore, may be selected specifically in the infant, despite the same CTL specificity being present in the mother. Additionally, pediatric CTL activity may be compromised both by the transmission of maternal escape variants and by mother-to-child transmission of escape variants that originally arose in the father. The unique acquisition of these CTL escape forms may help to explain the severe nature of some pediatric HIV infections.

摘要

细胞毒性T淋巴细胞(CTL)逃逸在快速进展的婴儿1型人类免疫缺陷病毒(HIV-1)感染中的作用尚不清楚。此处呈现的数据表明,婴儿HIV-1特异性CTL可在生命早期就选择出病毒逃逸变异株。此外,尽管母亲体内存在相同的CTL特异性,但这些变异株可能在婴儿体内被特异性选择。另外,母体逃逸变异株的传播以及最初在父亲体内出现的逃逸变异株的母婴传播,都可能损害儿童的CTL活性。这些CTL逃逸形式的独特获得情况可能有助于解释某些儿童HIV感染的严重性质。

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Not all tetramer binding CD8+ T cells can produce cytokines and chemokines involved in the effector functions of virus-specific CD8+ T lymphocytes in HIV-1 infected children.并非所有与四聚体结合的CD8+ T细胞都能产生参与HIV-1感染儿童中病毒特异性CD8+ T淋巴细胞效应功能的细胞因子和趋化因子。
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