Influenza A virus neuraminidase limits viral superinfection
Influenza A virus neuraminidase limits viral superinfection
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DOI：
10.1128/jvi.00079-08
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发表时间：
2008-05-01
影响因子：
5.4
通讯作者：
Farzan, Michael
中科院分区：
文献类型：
--
作者：
Huang, I-Chueh;Li, Wenhui;Farzan, Michael
包膜病毒利用多种机制抑制一个以上病毒粒子对靶细胞的感染。这些机制可能对分节病毒的进化特别重要，因为排除重复感染可能限制病毒基因重组的频率。在这里，我们发现甲型流感病毒神经氨酸酶（NA）的细胞表达，而不是血凝素（HA）或M2质子泵，抑制HA假型逆转录病毒的进入。感染H1N1或H3N2甲型流感病毒的细胞对ha介导的感染和与第二种甲型流感病毒的重复感染同样难治。神经氨酸酶抑制剂奥司他韦和扎那米韦可挽救ha介导的进入和病毒重复感染。这些抑制剂还可以阻止在表达NA或感染甲型流感病毒的细胞中观察到的α -2,3-和α -2,6-链唾液酸的去除。我们的数据表明，在病毒蛋白中，NA单独限制了甲型流感病毒的重复感染。
Enveloped viruses use multiple mechanisms to inhibit infection of a target cell by more than one virion. These mechanisms may be of particular importance for the evolution of segmented viruses, because superinfection exclusion may limit the frequency of reassortment of viral genes. Here, we show that cellular expression of influenza A virus neuraminidase (NA), but not hemagglutinin (HA) or the M2 proton pump, inhibits entry of HA-pseudotyped retroviruses. Cells infected with H1N1 or H3N2 influenza A virus were similarly refractory to HA-mediated infection and to superinfection with a second influenza A virus. Both HA-mediated entry and viral superinfection were rescued by the neuraminidase inhibitors oseltamivir carboxylate and zanamivir. These inhibitors also prevented the removal of alpha-2,3- and alpha-2,6-linked sialic acid observed in cells expressing NA or infected with influenza A viruses. Our data indicate that NA alone among viral proteins limits influenza A virus superinfection.