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Respiratory syncytial virus (RSV) attachment and entry

Reactome ID: R-HSA-9820960

中文名称

呼吸道合胞病毒 (RSV) 附着和进入

通路描述

人类呼吸道合胞病毒 (RSV) 进入宿主细胞涉及病毒包膜蛋白与宿主细胞附着因子的相互作用,以及病毒膜与宿主细胞膜的融合。G 糖蛋白是附着蛋白,与宿主细胞表面分子相互作用,使 RSV 病毒颗粒能够结合其靶细胞。虽然 F 糖蛋白可能促进附着,但其主要功能是促进病毒和宿主细胞膜的融合。SH 蛋白对进入是可选的。参考文献请参见 Battles and McLellan 2019。

使用人类原代支气管上皮细胞培养物,已建立 RSV 高效感染支气管上皮细胞,并从腔面特异性靶向纤毛支气管上皮细胞。在缺乏免疫反应的情况下,RSV 不会引起明显的细胞病理学(Zhang et al. 2002)。

除了纤毛呼吸道上皮细胞外,RSV 还可感染粒细胞并导致中性粒细胞和嗜酸性粒细胞的基线凋亡延迟(Lindemans et al. 2006)。RSV 还可感染新生儿特异性调节 B 细胞,这可能有助于婴儿中病毒载量高和疾病严重程度(Zhivaki et al. 2017)。
英文描述
Respiratory syncytial virus (RSV) attachment and entry The entry of human respiratory syncytial virus (RSV) into host cells involves attachment of the virion to the host cell surface, through interaction of viral envelope proteins with host cell attachment factors, and fusion of the viral membrane with the host cell membrane. The G glycoprotein is the attachment protein that interacts with surface molecules of the host cells, enabling the RSV virions to bind to their target cells. While the F glycoprotein may facilitate attachment, its primary function is to promote fusion of the viral and host cell membranes. The SH protein is dispensable for entry. For review, please refer to Battles and McLellan 2019.

Using human primary airway epithelial cell cultures, it was established that RSV efficiently infects the airway epithelium from the luminal surface and specifically targets ciliated airway epithelial cells. In the absence of immune response, RSV causes no obvious cytopathology (Zhang et al. 2002).

In addition to ciliated respiratory epithelial cells, RSV may infect granulocytes and cause a delay in constitutive apoptosis of neutrophils and eosinophils (Lindemans et al. 2006). RSV can also infect neonatal-specific regulatory B cells, which may contribute to high viral load and disease severity in infants (Zhivaki et al. 2017).

所含基因

13 个基因