Grunert H P, Wolf K U, Langner K D, Sawitzky D, Habermehl K O, Zeichhardt H
Institut für Klinische und Experimentelle Virologie, Universitätsklinikum Benjamin Franklin, Freie Universität Berlin, Germany.
Med Microbiol Immunol. 1997 Jun;186(1):1-9. doi: 10.1007/s004300050039.
Virus adsorption and uptake of human rhinovirus 14 (HRV14) were studied with HeLa cells and baby hamster kidney (BHK) cells which were transfected with the HRV14 receptor intercellular adhesion molecule-1 (ICAM-1). Transmission electron microscopy of HeLa cells revealed that HRV14 was internalized via clathrin-coated pits and -coated vesicles. A minority of virus particles also used uncoated vesicles for entry. The internalization showed the characteristics of receptor-mediated endocytosis. Presence of the carboxylic ionophore monensin inhibited viral uncoating, indicating a pH-dependent entry mechanism. The expression of ICAM-1 on the surface of the ICAM-1 transfected baby hamster kidney cells (BHK-ICAM cells) allowed extensive virus adsorption and internalization through membrane channels. Virus particles were lined up in these channels like pearls on a string, but did not induce a productive infection. Although ICAM-1 was expressed to the same degree on BHK-ICAM and HeLa cells, HRV14 induced neither viral protein and RNA syntheses nor infectious virus progeny in BHK-ICAM cells. ICAM-1 on the transfected BHK cells was a functional active receptor as it rendered these cells permissive to coxsackievirus A21. These results suggest that HRV14 uptake into BHK-ICAM cells is blocked directly in or shortly after its final step of internalization, the uncoating. Our findings underline that the receptor ICAM-1 determines virus uptake into cells, however, is not sufficient to confer susceptibility of BHK cells to HRV14 infection.
利用转染了人鼻病毒14型（HRV14）受体细胞间黏附分子-1（ICAM-1）的HeLa细胞和幼仓鼠肾（BHK）细胞，研究了HRV14的病毒吸附和摄取情况。对HeLa细胞进行透射电子显微镜观察发现，HRV14通过网格蛋白包被的小窝和包被小泡内化。少数病毒颗粒也利用未包被的小泡进入细胞。这种内化显示出受体介导的内吞作用的特征。羧酸离子载体莫能菌素的存在抑制了病毒脱壳，表明存在pH依赖性的进入机制。ICAM-1转染的幼仓鼠肾细胞（BHK-ICAM细胞）表面ICAM-1的表达使得病毒能够通过膜通道进行广泛的吸附和内化。病毒颗粒像串在绳子上的珍珠一样排列在这些通道中，但并未引发 productive感染。尽管ICAM-1在BHK-ICAM细胞和HeLa细胞上的表达程度相同，但HRV14在BHK-ICAM细胞中既未诱导病毒蛋白和RNA合成，也未产生有感染性的病毒后代。转染的BHK细胞上的ICAM-1是一种功能性活性受体，因为它使这些细胞对柯萨奇病毒A21敏感。这些结果表明，HRV14进入BHK-ICAM细胞在其内化的最后一步即脱壳过程中或之后不久被直接阻断。我们的研究结果强调，受体ICAM-1决定病毒进入细胞，但不足以使BHK细胞对HRV14感染敏感。 （注：原文中“productive infection”直译为“有生产性的感染”，在医学语境中可理解为能产生子代病毒等有效感染的情况，这里保留英文待进一步结合专业知识准确理解其含义；“lined up in these channels like pearls on a string”直译为“像串在绳子上的珍珠一样排列在这些通道中”；整体译文尽量忠实原文表述。）
