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在生产性感染的细胞中,长臂猿白血病病毒和双嗜性鼠白血病病毒的受体没有下调。

The receptors for gibbon ape leukemia virus and amphotropic murine leukemia virus are not downregulated in productively infected cells.

机构信息

National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892, USA.

出版信息

Retrovirology. 2011 Jul 5;8:53. doi: 10.1186/1742-4690-8-53.

DOI:10.1186/1742-4690-8-53
PMID:21729311
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3136417/
Abstract

BACKGROUND

Over the last several decades it has been noted, using a variety of different methods, that cells infected by a specific gammaretrovirus are resistant to infection by other retroviruses that employ the same receptor; a phenomenon termed receptor interference. Receptor masking is thought to provide an earlier means of blocking superinfection, whereas receptor down regulation is generally considered to occur in chronically infected cells.

RESULTS

We used replication-competent GFP-expressing viruses containing either an amphotropic murine leukemia virus (A-MLV) or the gibbon ape leukemia virus (GALV) envelope. We also constructed similar viruses containing fluorescence-labeled Gag proteins for the detection of viral particles. Using this repertoire of reagents together with a wide range of antibodies, we were able to determine the presence and availability of viral receptors, and detect viral envelope proteins and particles presence on the cell surface of chronically infected cells.

CONCLUSIONS

A-MLV or GALV receptors remain on the surface of chronically infected cells and are detectable by respective antibodies, indicating that these receptors are not downregulated in these infected cells as previously proposed. We were also able to detect viral envelope proteins on the infected cell surface and infected cells are unable to bind soluble A-MLV or GALV envelopes indicating that receptor binding sites are masked by endogenously expressed A-MLV or GALV viral envelope. However, receptor masking does not completely prevent A-MLV or GALV superinfection.

摘要

背景

在过去几十年中,人们使用各种不同的方法发现,被特定γ逆转录病毒感染的细胞对使用相同受体的其他逆转录病毒的感染具有抗性;这一现象被称为受体干扰。受体遮蔽被认为是一种更早阻止超感染的手段,而受体下调通常被认为发生在慢性感染的细胞中。

结果

我们使用含有双嗜性鼠白血病病毒(A-MLV)或长臂猿白血病病毒(GALV)包膜的复制型 GFP 表达病毒。我们还构建了类似的病毒,用于检测病毒颗粒的荧光标记 Gag 蛋白。使用这一系列试剂以及广泛的抗体,我们能够确定病毒受体的存在和可用性,并检测慢性感染细胞表面病毒包膜蛋白和颗粒的存在。

结论

A-MLV 或 GALV 受体仍然存在于慢性感染细胞的表面,并可被相应的抗体检测到,这表明这些受体在这些感染细胞中并未下调,如先前提出的那样。我们还能够在感染细胞表面检测到病毒包膜蛋白,并且感染细胞不能结合可溶性 A-MLV 或 GALV 包膜,表明受体结合位点被内源性表达的 A-MLV 或 GALV 病毒包膜遮蔽。然而,受体遮蔽并不能完全阻止 A-MLV 或 GALV 的超感染。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59eb/3136417/0f65b7f4a1d9/1742-4690-8-53-8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59eb/3136417/51e1d183f9be/1742-4690-8-53-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59eb/3136417/4acade65c563/1742-4690-8-53-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59eb/3136417/faedb9b2b873/1742-4690-8-53-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59eb/3136417/6f7f9897cefd/1742-4690-8-53-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59eb/3136417/cf4dc35ceae4/1742-4690-8-53-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59eb/3136417/8232e6e313c4/1742-4690-8-53-6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59eb/3136417/234219144a14/1742-4690-8-53-7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59eb/3136417/0f65b7f4a1d9/1742-4690-8-53-8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59eb/3136417/51e1d183f9be/1742-4690-8-53-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59eb/3136417/4acade65c563/1742-4690-8-53-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59eb/3136417/faedb9b2b873/1742-4690-8-53-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59eb/3136417/6f7f9897cefd/1742-4690-8-53-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59eb/3136417/cf4dc35ceae4/1742-4690-8-53-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59eb/3136417/8232e6e313c4/1742-4690-8-53-6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59eb/3136417/234219144a14/1742-4690-8-53-7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59eb/3136417/0f65b7f4a1d9/1742-4690-8-53-8.jpg

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