Human parainfluenza virus type 2 polymerase complex recognizes leader promoters of other species belonging to the genus Rubulavirus
Human parainfluenza virus type 2 polymerase complex recognizes leader promoters of other species belonging to the genus Rubulavirus
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人类副流感病毒 2 型聚合酶复合物可识别属于风疹病毒属其他物种的前导启动子
DOI：
10.1007/s00430-017-0520-3
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发表时间：
2017
期刊：
影响因子：
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通讯作者：
Nishio Machiko
中科院分区：
文献类型：
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作者：
Matsumoto Yusuke;Ohta Keisuke;Nishio Machiko
副粘病毒的前导序列位于病毒基因组的3′端，决定着病毒转录和复制的程度。然而，前导序列中影响病毒繁殖的必要核苷酸尚未详细研究。在本研究中，我们发现，人副流感病毒2型（hPIV2）的聚合酶复合体使用的是一个编码内切酶的hPIV2微型基因组，该基因组具有来自其他密切相关病毒的前导序列作为模板。此外，我们证明，虽然hPIV2聚合酶复合物可以识别hPIV4B，腮腺炎病毒（MuV）和PIV 5以及纽卡斯尔病病毒（NDV）的前导序列，但它不能识别麻疹病毒，hPIV1，仙台病毒（SeV）或hPIV3。我们可以获得具有hPIV4B、MuV和PIV5的前导序列的嵌合hPIV2，而不能获得来自其他种属（包括NDV和SeV）的嵌合hPIV2。这些结果表明，虽然hPIV2聚合酶复合物可以识别来自风疹病毒的前导序列以实现有效的病毒感染，但这不适用于属于其他属的病毒。副粘病毒之间前导序列核苷酸的比较突出了前13个核苷酸的保守性对感染性hPIV 2生长的重要性。
Leader sequence, located at the 3′ terminus of paramyxovirus genomes, determines the degree of viral transcription and replication. The essential nucleotides in the leader sequence that influence viral propagation, however, have not been investigated in detail. In the present study, we show that polymerase complex of human parainfluenza virus type 2 (hPIV2) uses a luciferase-encoding hPIV2 mini-genome possessing the leader sequence from other closely related viruses as a template. Furthermore, we demonstrate that although hPIV2 polymerase complex can recognize the leader sequence of hPIV4B, mumps virus (MuV) and PIV5 as well as Newcastle disease virus (NDV), it cannot recognize measles virus, hPIV1, Sendai virus (SeV) or hPIV3. We could obtain the chimeric hPIV2 possessing the leader sequence from hPIV4B, MuV and PIV5, but not from other species, including NDV and SeV. These results reveal that although hPIV2 polymerase complex can recognize the leader sequence from rubulaviruses to achieve efficient viral infection, this does not apply to viruses belonging to other genus. A comparison of leader sequence nucleotides among paramyxoviruses highlights the importance of the conservation in the first 13 nucleotides for infectious hPIV2 growth.