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.<br><br>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).<br><br>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).

人类呼吸道合胞病毒（RSV）进入宿主细胞的过程涉及病毒颗粒与宿主细胞表面的附着，这一过程通过病毒包膜蛋白与宿主细胞附着因子的相互作用来实现，以及病毒膜与宿主细胞膜的融合。G糖蛋白作为附着蛋白，与宿主细胞的表面分子相互作用，使得RSV病毒颗粒能够与其靶细胞结合。尽管F糖蛋白可能有助于附着，但其主要功能是促进病毒膜与宿主细胞膜的融合。SH蛋白对于进入过程并非必需。欲深入了解，请参阅 Battles 和 McLellan 于 2019 年发表的相关综述。<br><br>利用人原代气道上皮细胞培养，已证实RSV能够从腔面高效感染气道上皮细胞，并特异性地靶向纤毛上皮细胞。在缺乏免疫反应的情况下，RSV不会引起明显的细胞病理学变化（参见 Zhang 等人于 2002 年的研究）。<br><br>除了纤毛呼吸道上皮细胞外，RSV还可能感染粒细胞，导致中性粒细胞和嗜酸性粒细胞的构成性凋亡延迟（参见 Lindemans 等人于 2006 年的研究）。RSV亦能感染新生儿特异性的调节B细胞，这或许会导致婴儿病毒载量升高和疾病严重程度增加（参见 Zhivaki 等人于 2017 年的研究）。