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Vaccine. 2005 Apr 22;23(22):2922-7. doi: 10.1016/j.vaccine.2004.11.058.
2
Influenza virus entry and infection require host cell N-linked glycoprotein.流感病毒的进入和感染需要宿主细胞的N-连接糖蛋白。
Proc Natl Acad Sci U S A. 2004 Dec 28;101(52):18153-8. doi: 10.1073/pnas.0405172102. Epub 2004 Dec 15.
3
Characterization of a neuraminidase-deficient influenza a virus as a potential gene delivery vector and a live vaccine.一种神经氨酸酶缺陷型甲型流感病毒作为潜在基因递送载体和活疫苗的特性研究
J Virol. 2004 Mar;78(6):3083-8. doi: 10.1128/jvi.78.6.3083-3088.2004.
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N-glycosylation is required for the surface localization of MUC17 mucin.N-糖基化是MUC17粘蛋白表面定位所必需的。
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A release-competent influenza A virus mutant lacking the coding capacity for the neuraminidase active site.一种缺乏神经氨酸酶活性位点编码能力的具有释放能力的甲型流感病毒突变体。
J Gen Virol. 2002 Nov;83(Pt 11):2683-2692. doi: 10.1099/0022-1317-83-11-2683.
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Proc Natl Acad Sci U S A. 2002 Oct 15;99(21):13849-54. doi: 10.1073/pnas.212519699. Epub 2002 Oct 4.
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Functional balance between haemagglutinin and neuraminidase in influenza virus infections.流感病毒感染中血凝素与神经氨酸酶之间的功能平衡。
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Involvement of VIP36 in intracellular transport and secretion of glycoproteins in polarized Madin-Darby canine kidney (MDCK) cells.血管活性肠肽36（VIP36）参与极化的犬肾上皮细胞（MDCK细胞）中糖蛋白的细胞内运输和分泌。
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N-Glycans attached to the stem domain of haemagglutinin efficiently regulate influenza A virus replication.附着于血凝素茎区的N-聚糖可有效调节甲型流感病毒的复制。
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血凝素糖基化对流感病毒对神经氨酸酶抑制剂敏感性的影响。

Effect of hemagglutinin glycosylation on influenza virus susceptibility to neuraminidase inhibitors.

作者信息

Mishin Vasiliy P, Novikov Dmitri, Hayden Frederick G, Gubareva Larisa V

机构信息

Department of Internal Medicine, School of Medicine, University of Virginia, Charlottesville, VA, USA.

出版信息

J Virol. 2005 Oct;79(19):12416-24. doi: 10.1128/JVI.79.19.12416-12424.2005.

DOI:10.1128/JVI.79.19.12416-12424.2005
PMID:16160169
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1211522/
Abstract

Inhibition of neuraminidase (NA) activity prevents release of progeny virions from influenza-infected cells and removal of neuraminic (sialic) acid moieties from glycans attached to hemagglutinin (HA). Neuraminic acid moieties situated near the HA receptor-binding site can reduce the efficiency of virus binding and decrease viral dependence on NA activity for replication. With the use of reverse genetics technique, we investigated the effect of glycans attached at Asn 94a, 129, and 163 on the virus susceptibility to NA inhibitors in MDCK cells and demonstrated that the glycan attached at Asn 163 plays a dominant role in compensation for the loss of NA activity.

摘要

抑制神经氨酸酶（NA）活性可阻止子代病毒粒子从流感感染细胞中释放，并阻止从附着于血凝素（HA）的聚糖上去除神经氨酸（唾液酸）部分。位于HA受体结合位点附近的神经氨酸部分可降低病毒结合效率，并降低病毒复制对NA活性的依赖性。利用反向遗传学技术，我们研究了天冬酰胺94a、129和163处连接的聚糖对MDCK细胞中病毒对NA抑制剂敏感性的影响，并证明天冬酰胺163处连接的聚糖在补偿NA活性丧失方面起主要作用。