Host range restriction of parainfluenza virus growth occurs at the level of virus genome replication.
Host range restriction of parainfluenza virus growth occurs at the level of virus genome replication.
复制标题
副流感病毒生长的宿主范围限制发生在病毒基因组复制水平上。
DOI：
10.1006/viro.1996.0287
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Ryan,KW
中科院分区：
文献类型：
--
作者：
Tao,T;Ryan,KW
为了阐明副流感病毒复制宿主范围限制的分子基础，我们研究了人副流感病毒1型（hPIV 1）在非允许MDBK细胞流产感染过程中产生的病毒大分子类型。虽然这些细胞不支持hPIV 1病毒的产生，但它们可被hPIV 1感染，如细胞内病毒NP和HN蛋白的蓄积所证明。HPIV 1还能够驱动转染到病毒感染的MDBK细胞中的仙台病毒（SV）基因组RNA的合成类似物的转录。与转录相反，MDBK细胞中不发生hPIV 1基因组复制。细胞内全长基因组RNA在感染后2天仅检测到痕量，并且在感染后4天检测不到。未检测到全长反基因组（+）正义RNA。核衣壳复合物未能积累在nonpermissive细胞的细胞质中，没有检测到的核衣壳释放到介质中的病毒颗粒。数据表明，vRNA合成和/或核衣壳形成缺陷是hPIV 1无法在MDBK细胞中生长的原因。我们的数据还表明，hPIV 1能够提供所有辅助功能，用于将SV合成基因组类似物包装成感染性颗粒，但这些与hPIV 1蛋白结合的SV特异性RNA反过来不会被SV蛋白复制。这些结果表明，副流感病毒株之间的功能性蛋白质-蛋白质相互作用比蛋白质-RNA相互作用有更严格的要求。
To illuminate the molecular basis for host range restriction of parainfluenza virus replication, we have examined the types of virus macromolecules produced during abortive infection of nonpermissive MDBK cells with human parainfluenza virus type 1 (hPIV1). While these cells do not support production of hPIV1 virus, they can be infected by hPIV1 as evidenced by accumulation of intracellular viral NP and HN proteins. HPIV1 is also able to drive transcription of a synthetic analog of Sendai virus (SV) genome RNA transfected into virus-infected MDBK cells. In contrast to transcription, hPIV1 genome replication does not occur in MDBK cells. Intracellular full-length genome RNA was detected only in trace amounts 2 days after infection, and was undetectable 4 days after infection. Full-length antigenome (+) sense RNA was not detectable. Nucleocapsid complexes failed to accumulate in the cytoplasm of nonpermissive cells, and no detectable nucleocapsids were released into the medium as virus particles. The data indicate that defective vRNA synthesis and/or nucleocapsid formation is responsible for the inability of hPIV1 to grow in MDBK cells. Our data also show that hPIV1 is capable of providing all helper functions for packaging SV synthetic genome analogs into infectious particles, but these SV-specific RNAs encapsidated with hPIV1 proteins are in turn not replicated by SV proteins. These results suggest that functional protein–protein interactions between parainfluenza virus strains have more stringent requirements than do protein–RNA interactions.