Mouse cells expressing human intercellular adhesion molecule-1 are susceptible to infection by coxsackievirus A21
Mouse cells expressing human intercellular adhesion molecule-1 are susceptible to infection by coxsackievirus A21
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DOI：
10.1128/jvi.71.1.785-789.1997
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发表时间：
1997-01-01
影响因子：
5.4
通讯作者：
Barry, RD
中科院分区：
文献类型：
--
作者：
Shafren, DR;Dorahy, DJ;Barry, RD
以前的竞争性病毒结合分析表明，柯萨奇病毒A21(CAV21)和人鼻病毒14(HRV14)具有共同的细胞表面受体。最近，细胞间黏附分子-1(ICAM-1)被确定为HRV-14的细胞受体。此外，抗ICAM-1的单抗(MAb)阻断了HRV14、CAV13、CAV18和CAV21的感染，表明这些病毒共享这种受体；然而，这一点从未通过更直接的方法得到证实。在这项研究中，我们最终证明CAV21与ICAM-1结合，针对分子N-末端结构域的单抗抑制这种结合。此外，我们还证明了ICAM-1与160S CAV21病毒粒子之间的特异性相互作用诱导了135S A粒子的形成。最后，我们发现，将人ICAM-1基因导入正常不敏感的小鼠L细胞，使其对CAV21感染易感。
Competitive viral binding assays have revealed previously that coxsackievirus A21 (CAV21) and human rhinovirus 14 (HRV14) share a common cell surface receptor. More recently, intercellular adhesion molecule-1 (ICAM-1) has been identified as the cellular receptor for HRV-14. Also, anti-ICAM-1 monoclonal antibodies (MAbs) blocked infection by HRV14, CAV13, CAV18, and CAV21, suggesting that these viruses share this receptor; however, this has never been established by more direct methods. In this study we show conclusively that CAV21 binds to ICAM-1 and that MAbs directed against the N-terminal domain of the molecule inhibit this attachment. Furthermore, we show that the specific interaction between ICAM-1 and 160S CAV21 virions induces formation of 135S A particles. Finally, we show transfection of normally nonsusceptible mouse L cells with human ICAM-1 cDNA renders them susceptible to infection by CAV21.