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广泛的HIV-1宿主内重组在组织病理学异常的组织中很常见。

Extensive HIV-1 intra-host recombination is common in tissues with abnormal histopathology.

作者信息

Lamers Susanna L, Salemi Marco, Galligan Derek C, de Oliveira Tulio, Fogel Gary B, Granier Sara C, Zhao Li, Brown Joseph N, Morris Alanna, Masliah Eliezer, McGrath Michael S

机构信息

BioInfoExperts, Thibodaux, LA, USA.

出版信息

PLoS One. 2009;4(3):e5065. doi: 10.1371/journal.pone.0005065. Epub 2009 Mar 31.

DOI:10.1371/journal.pone.0005065
PMID:19333384
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2659430/
Abstract

There is evidence that immune-activated macrophages infected with the Human Immunodeficiency Virus (HIV) are associated with tissue damage and serve as a long-lived viral reservoir during therapy. In this study, we analyzed 780 HIV genetic sequences generated from 53 tissues displaying normal and abnormal histopathology. We found up to 50% of the sequences from abnormal lymphoid and macrophage rich non-lymphoid tissues were intra-host viral recombinants. The presence of extensive recombination, especially in non-lymphoid tissues, implies that HIV-1 infected macrophages may significantly contribute to the generation of elusive viral genotypes in vivo. Because recombination has been implicated in immune evasion, the acquisition of drug-resistance mutations, and alterations of viral co-receptor usage, any attempt towards the successful eradication of HIV-1 requires therapeutic approaches targeting tissue macrophages.

摘要

有证据表明,感染人类免疫缺陷病毒(HIV)的免疫激活巨噬细胞与组织损伤有关,并在治疗期间作为一个长期的病毒储存库。在本研究中,我们分析了从53个显示正常和异常组织病理学的组织中产生的780个HIV基因序列。我们发现,来自异常淋巴组织和富含巨噬细胞的非淋巴组织的序列中,高达50%是宿主内病毒重组体。广泛重组的存在,特别是在非淋巴组织中,意味着HIV-1感染的巨噬细胞可能在体内显著促成难以捉摸的病毒基因型的产生。由于重组与免疫逃避、耐药性突变的获得以及病毒共受体使用的改变有关,任何成功根除HIV-1的尝试都需要针对组织巨噬细胞的治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c525/2659430/496208bc880e/pone.0005065.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c525/2659430/fdb7f87e716a/pone.0005065.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c525/2659430/d6aab3a8c1f3/pone.0005065.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c525/2659430/f5a7fc13ea03/pone.0005065.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c525/2659430/985c54125e43/pone.0005065.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c525/2659430/496208bc880e/pone.0005065.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c525/2659430/fdb7f87e716a/pone.0005065.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c525/2659430/d6aab3a8c1f3/pone.0005065.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c525/2659430/f5a7fc13ea03/pone.0005065.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c525/2659430/985c54125e43/pone.0005065.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c525/2659430/496208bc880e/pone.0005065.g005.jpg

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