Tao T, Ryan K W
Department of Virology and Molecular Biology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.
Virology. 1996 Jun 1;220(1):69-77. doi: 10.1006/viro.1996.0287.
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.
为阐明副流感病毒复制宿主范围限制的分子基础，我们检测了用1型人副流感病毒（hPIV1）对非允许性MDBK细胞进行流产感染期间产生的病毒大分子类型。虽然这些细胞不支持hPIV1病毒的产生，但它们可被hPIV1感染，细胞内病毒核蛋白（NP）和血凝素神经氨酸酶（HN）蛋白的积累证明了这一点。hPIV1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合成类似物的转录。与转录不同，hPIV1基因组复制在MDBK细胞中不发生。感染后2天仅检测到微量的细胞内全长基因组RNA，感染后4天则无法检测到。全长反基因组（+）链RNA无法检测到。核衣壳复合物未能在非允许性细胞的细胞质中积累，并且没有可检测到的核衣壳作为病毒颗粒释放到培养基中。数据表明，有缺陷的病毒RNA（vRNA）合成和/或核衣壳形成是hPIV1无法在MDBK细胞中生长的原因。我们的数据还表明，hPIV1能够提供所有辅助功能，将SV合成基因组类似物包装成感染性颗粒，但这些被hPIV1蛋白包裹的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。
