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α干扰素对T细胞中1型人类免疫缺陷病毒形态发生的抑制作用。

Inhibition of human immunodeficiency virus type 1 morphogenesis in T cells by alpha interferon.

作者信息

Smith M S, Thresher R J, Pagano J S

机构信息

Lineberger Cancer Research Center, University of North Carolina, Chapel Hill 27599-7295.

出版信息

Antimicrob Agents Chemother. 1991 Jan;35(1):62-7. doi: 10.1128/AAC.35.1.62.

DOI:10.1128/AAC.35.1.62
PMID:1707604
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC244942/
Abstract

Some murine retroviruses exhibit altered release of virus when cells are treated with alpha interferon (IFN-alpha), resulting in the accumulation of intracellular virions in cytoplasmic vacuoles. In studies of the inhibitory effect of IFN-alpha (Wellferon) on acute human immunodeficiency virus type 1 infection of human T-cell lines, we found that in C3 cells, the 50% effective concentration was 9 U/ml and the 90% effective concentration was 310 U/ml. There was no apparent accumulation of intracellular particles detected by p24 antigen levels or by processing the cells for electron microscopy. Extracellular reverse transcriptase activity and p24 levels decreased in parallel with increasing IFN, whereas the intracellular viral proteins decreased only slightly. By electron microscopy, cells treated with higher concentrations of IFN (512 U/ml) disclosed very few particles budding into extracellular spaces; no intracellular particles could be seen, despite nearly normal levels of intracellular viral protein detected by the p24 antigen assay and correct processing detected by Western blot (immunoblot) analysis. Thus in human immunodeficiency virus-infected cells, the major block produced by IFN-alpha appeared to be late in the viral cycle at the morphogenesis stage of virion production. Chronically infected Jurkat cells treated with IFN appeared to be inhibited in growth rate, as virus production decreased proportionally with cell number.

摘要

当细胞用α干扰素(IFN-α)处理时,一些鼠逆转录病毒会出现病毒释放改变的情况,导致细胞质空泡中细胞内病毒粒子的积累。在关于IFN-α(Wellferon)对人T细胞系急性人类免疫缺陷病毒1型感染的抑制作用的研究中,我们发现,在C3细胞中,50%有效浓度为9 U/ml,90%有效浓度为310 U/ml。通过p24抗原水平或对细胞进行电子显微镜处理,未检测到细胞内颗粒有明显积累。细胞外逆转录酶活性和p24水平随着IFN浓度增加而平行下降,而细胞内病毒蛋白仅略有下降。通过电子显微镜观察,用较高浓度IFN(512 U/ml)处理的细胞显示出很少有颗粒出芽进入细胞外空间;尽管通过p24抗原检测法检测到细胞内病毒蛋白水平近乎正常,且通过蛋白质印迹(免疫印迹)分析检测到处理正确,但未见细胞内颗粒。因此,在人类免疫缺陷病毒感染的细胞中,IFN-α产生的主要阻断作用似乎发生在病毒周期后期病毒粒子产生的形态发生阶段。用IFN处理的慢性感染Jurkat细胞的生长速率似乎受到抑制,因为病毒产生与细胞数量成比例下降。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/daa2/244942/4501ecb6c323/aac00046-0107-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/daa2/244942/1c622dc4d4cc/aac00046-0106-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/daa2/244942/4501ecb6c323/aac00046-0107-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/daa2/244942/1c622dc4d4cc/aac00046-0106-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/daa2/244942/4501ecb6c323/aac00046-0107-a.jpg

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