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减毒鼠巨细胞病毒与N-乙酰葡糖胺结合，向毒力的转变可能涉及唾液酸的识别。

Attenuated murine cytomegalovirus binds to N-acetylglucosamine, and shift to virulence may involve recognition of sialic acids.

作者信息

Ravindranath R M, Graves M C

机构信息

Department of Neurology, Reed Neurological Research Center, UCLA School of Medicine 90024-1769.

出版信息

J Virol. 1990 Nov;64(11):5430-40. doi: 10.1128/JVI.64.11.5430-5440.1990.

DOI:10.1128/JVI.64.11.5430-5440.1990
PMID:2170680
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC248594/
Abstract

Treatment of cells with lectins specific for N-acetylglucosamine (GlcNAc) blocked infection by mouse cytomegalovirus (MCMV), and GlcNAc pretreatment of the lectin blocked this effect. MCMV failed to infect N-acetylglucosaminidase (GlcNAcase)-treated mouse embryo fibroblasts (MEF). GlcNAc and GlcNAc-containing synthetic oligosaccharides directly inhibited viral infectivity. Ulex lectin inhibition of infection was shown to be due to inhibition of surface adsorption of 35S-labeled virus. Also, GlcNAcase eluted 35S-labeled virus adsorbed to MEF at 4 degrees C and inhibited plaque formation if added after adsorption at this temperature. These findings indicate that GlcNAc binding is involved in attachment rather than in some later step in infection. High-performance thin-layer chromatography overlay of [35S]MCMV indicated that it binds to a GlcNAc-containing asialoglycolipid. Analogous experiments indicated that MCMV made virulent by in vivo salivary gland passage binds to sialic acids in addition to GlcNAc. Treatment of MEF with sialic acid-binding lectins blocked infectivity. Incubation of virus with sialic acids also prevented infection. N-acetylneuraminic acid was 10(3)-fold more potent than N-glycolylneuraminic acid. Sialidase-treated target cells were not efficiently infected by the virus. Thus, MCMV binds to GlcNAc on the cell surface, and the shift to virulence (by in vivo salivary gland passage) correlates with viral recognition of sialic acids.

摘要

用对N - 乙酰葡糖胺（GlcNAc）具有特异性的凝集素处理细胞可阻断小鼠巨细胞病毒（MCMV）的感染，并且凝集素的GlcNAc预处理可阻断这种效应。MCMV无法感染经N - 乙酰葡糖胺酶（GlcNAcase）处理的小鼠胚胎成纤维细胞（MEF）。GlcNAc和含GlcNAc的合成寡糖可直接抑制病毒感染性。已证明荆豆凝集素对感染的抑制是由于抑制了35S标记病毒的表面吸附。此外，GlcNAcase可洗脱在4℃吸附于MEF的35S标记病毒，并且如果在此温度下吸附后添加则可抑制噬斑形成。这些发现表明GlcNAc结合参与了病毒附着，而不是感染的某些后续步骤。[35S]MCMV的高效薄层层析覆盖表明它与一种含GlcNAc的去唾液酸糖脂结合。类似实验表明，经体内唾液腺传代而致毒的MCMV除了结合GlcNAc外还结合唾液酸。用结合唾液酸的凝集素处理MEF可阻断感染性。病毒与唾液酸孵育也可防止感染。N - 乙酰神经氨酸的效力比N - 羟乙酰神经氨酸高10³倍。经唾液酸酶处理的靶细胞不能被病毒有效感染。因此，MCMV在细胞表面结合GlcNAc，并且向毒力的转变（通过体内唾液腺传代）与病毒对唾液酸的识别相关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ad4/248594/0701996b9c93/jvirol00066-0215-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ad4/248594/25e0726f3e0c/jvirol00066-0215-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ad4/248594/0701996b9c93/jvirol00066-0215-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ad4/248594/25e0726f3e0c/jvirol00066-0215-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ad4/248594/0701996b9c93/jvirol00066-0215-b.jpg

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