Influenza A virus utilizes suboptimal splicing to coordinate the timing of infection.
Influenza A virus utilizes suboptimal splicing to coordinate the timing of infection.
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DOI：
10.1016/j.celrep.2012.12.010
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发表时间：
2013-01-31
期刊：
影响因子：
8.8
通讯作者：
Tenoever BR
中科院分区：
文献类型：
--
作者：
Chua MA;Schmid S;Perez JT;Langlois RA;Tenoever BR
Influenza A virus is unique as an RNA virus in that it replicates in the nucleus and undergoes splicing. With only ten major proteins, the virus must gain nuclear access, replicate, assemble progeny virions in the cytoplasm and then egress. In an effort to elucidate the coordination of these events, we manipulated the transcript levels from the bicistronic NS segment that encodes the spliced virus product responsible for genomic nuclear export. We find that utilization of an erroneous splice site ensures the slow accumulation of the viral Nuclear Export Protein (NEP) while generating excessive levels of an antagonist designed to inhibit the cellular response to infection. Modulation of this simple transcriptional event results in improperly timed export and loss of virus infection. Together, these data demonstrate that coordination of the influenza A virus life cycle is set by a ‘molecular timer’ that operates on the inefficient splicing of a virus transcript.
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