Virus-receptor interactions of human parainfluenza viruses types 1, 2 and 3
Virus-receptor interactions of human parainfluenza viruses types 1, 2 and 3
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DOI：
10.1006/mpat.1999.0313
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发表时间：
1999-11-01
影响因子：
3.8
通讯作者：
Moscona, A
中科院分区：
文献类型：
--
作者：
Ah-Tye, C;Schwartz, S;Moscona, A
人类副流感病毒1、2和3型（HPF 1、2和3型）是儿童的重要病原体。虽然这些病毒具有共同的结构和复制策略，但它们针对的是呼吸道的不同部位；HPF3感染最常见的结果是毛细支气管炎和肺炎，而hpf1和hpf2与组相关。虽然HPF3融合蛋白(F)对膜融合至关重要，但我们之前的工作表明，受体结合血凝素-神经氨酸酶（HN）在融合过程中也是必不可少的，HN与其细胞表面含唾液酸受体之间的相互作用是HPF3介导的细胞融合所必需的。利用我们对hpf3hn在细胞结合和病毒进入过程中的功能的理解，我们正在研究hpf1和hpf2中这些过程的不同方式，部分是通过操纵受体的可用性。采用3个实验处理比较HPF 1、2和3对hn -受体的相互作用。感染多重性高（m.o.i.）；低moi感染细胞的细菌神经氨酸酶治疗低moi感染细胞的病毒神经氨酸酶治疗（使用新城疫病毒[NDV]神经氨酸酶或紫外线照射的HPF3作为神经氨酸酶的来源）。在感染HPF3的细胞中，我们已经证明，高m.o.i感染通过去除病毒HN的唾液酸受体来阻止融合。然而，在HPF 1和HPF 2感染的细胞中，高m.o.i.感染并未阻断融合；融合度随运动速度的增加而增加。在感染hpf1和2的细胞中，细菌和NDV神经氨酸酶都没有阻断细胞融合，使用的神经氨酸酶量完全阻断HPF3感染细胞的融合。然而，当灭活的HPF3作为病毒神经氨酸酶的来源时，治疗抑制了感染hpf1和2以及3的细胞的融合。这些病毒在与细胞的相互作用、调节细胞-细胞融合的能力和对各种特异性外源性神经氨酸酶的反应方面的差异，可能反映了这三种病毒在生物学特性上的显著差异。(C) 1999学术出版社。
Human parainfluenza viruses types 1, 2 and 3 (HPF 1, 2 and 3) are important pathogens in children. While these viruses share common structures and replication strategies, they target different parts of the respiratory tract; the most common outcomes of infection with HPF3 are bronchiolitis and pneumonia, while HPF 1 and 2 are associated with croup. While the HPF3 fusion protein (F) is critical for membrane fusion, our previous work revealed that the receptor binding hemagglutinin-neuraminidase (HN) is also essential to the fusion process, interaction between HN and its sialic acid-containing receptor on cell surfaces is required for HPF3 mediated cell fusion. Using our understanding of HPF3 HN's functions in the cell-binding and viral entry process, we are investigating the ways in which these processes differ in HPF 1 and 2, in part by manipulating receptor availability. Three experimental treatments were used to compare the HN-receptor interaction of HPF 1, 2 and 3. infection at high multiplicity of infection (m.o.i.); bacterial neuraminidase treatment of cells infected at low m.o.i.; and viral neuraminidase treatment of cells infected at low m.o.i. (using Newcastle disease virus [NDV] neuraminidase or UV irradiated HPF3 as sources of neuraminidase). In cells infected with HPF3, we have shown that infection with high m.o.i. blocks fusion, by removing sialic acid receptors for the viral HN. However, in cells infected with HPF 1 and 2, infection with high m.o.i. did not block fusion; the fusion increases with increasing m.o.i.. In cells infected with HPF 1 and 2, neither bacterial nor NDV neuraminidase blocked cell fusion, using amounts of neuraminidase that completely block fusion of HPF3 infected cells. However, when inactivated HPF3 was used as a source of viral neuraminidase, the treatment inhibited fusion of cells infected with HPF 1 and 2 as well as 3. The differences found between these viruses in terms of their interaction with the cell, ability to modulate cell-cell fusion and reponse to exogenous neuraminidases of various specificities, may reflect salient differences in biological properties of the three viruses. (C) 1999 Academic Press.