Huberman K, Peluso R W, Moscona A
Department of Pediatrics, Mount Sinai School of Medicine, New York, New York 10029-6574, USA.
Virology. 1995 Dec 1;214(1):294-300. doi: 10.1006/viro.1995.9925.
The function of neuraminidase in the life cycle and pathogenesis of human parainfluenza virus type 3 (HPF3) was studied by analyzing a variant of HPF3 that has decreased neuraminidase enzymatic activity. The variant virus is more fusogenic than the wild-type virus during an acute infection. Cloning and sequencing of the fusion (F) and hemagglutinin-neuraminidase (HN) genes from this variant revealed a single amino acid change in the HN protein and no alterations in the F protein sequence. Analysis of the growth properties of this variant revealed a delay in release of virus particles into the supernatant. Addition of exogenous neuraminidase to the culture resulted in increased release of infections viral particles, suggesting that the viral neuraminidase is important for release of HPF3 from the infected cell surface. In addition, the behavior of the variant virus during high-multiplicity infection and in the presence of exogenous neuraminidase provided evidence that the neuraminidase of HPF3 determines the outcome of viral infection (cytopathic versus persistent) in cell culture.
通过分析一种神经氨酸酶酶活性降低的3型人副流感病毒（HPF3）变体，研究了神经氨酸酶在HPF3生命周期和发病机制中的作用。在急性感染期间，该变体病毒比野生型病毒更具融合性。对该变体的融合（F）基因和血凝素神经氨酸酶（HN）基因进行克隆和测序，结果显示HN蛋白中有一个氨基酸发生了变化，而F蛋白序列没有改变。对该变体生长特性的分析表明，病毒颗粒释放到上清液中的过程有所延迟。向培养物中添加外源性神经氨酸酶会导致感染性病毒颗粒的释放增加，这表明病毒神经氨酸酶对于HPF3从受感染细胞表面释放至关重要。此外，该变体病毒在高倍感染期间以及在外源性神经氨酸酶存在的情况下的行为提供了证据，表明HPF3的神经氨酸酶决定了细胞培养中病毒感染的结果（细胞病变与持续性）。
