首页> 外文期刊>Virology >The coxsackie-adenovirus receptor (CAR) is used by reference strains and clinical isolates representing all six serotypes of coxsackievirus group B and by swine vesicular disease virus.
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The coxsackie-adenovirus receptor (CAR) is used by reference strains and clinical isolates representing all six serotypes of coxsackievirus group B and by swine vesicular disease virus.

机译:柯萨奇腺病毒受体(CAR)被代表B型柯萨奇病毒B组所有六种血清型的参考菌株和临床分离株以及猪水泡病病毒所使用。

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Group B coxsackieviruses are etiologically linked to many human diseases, and cell surface receptors are postulated to play an important role in mediating their pathogenesis. The coxsackievirus adenovirus receptor (CAR) has been shown to function as a receptor for selected strains of coxsackievirus group B (CVB) serotypes 3, 4, and 5 and is postulated to serve as a receptor for all six serotypes. In this study, we demonstrate that CAR can serve as a receptor for laboratory reference strains and clinical isolates of all six CVB serotypes. Infection of CHO cells expressing human CAR results in a 1000-fold increase in CVB progeny virus titer compared to mock transfected cells. CAR was shown to be a functional receptor for swine vesicular disease virus (SVDV), as CHO-CAR cells but not CHO mock transfected controls were susceptible to SVDV infection, produced progeny SVDV, and developed cytopathic effects. Moreover, SVDV infection could be specifically blocked by monoclonal antibody to CAR (RmcB). SVDV infection of HeLa cells was also inhibited by an anti-CD55 MAb, suggesting that this virus, like some CVB, may interact with CD55 (decay accelerating factor) in addition to CAR. Finally, pretreatment of CVB or SVDV with soluble CAR effectively blocks virus infection of HeLa cell monolayers. Copyright 2000 Academic Press.
机译:B型柯萨奇病毒在病因上与许多人类疾病相关,并且假定细胞表面受体在介导其发病机理中起重要作用。柯萨奇病毒腺病毒受体(CAR)已被证明可作为所选的柯萨奇病毒B组(CVB)血清型3、4和5的受体发挥作用,并被假定为所有六种血清型的受体。在这项研究中,我们证明CAR可以作为所有六种CVB血清型的实验室参考菌株和临床分离株的受体。与模拟转染的细胞相比,感染表达人CAR的CHO细胞会导致CVB后代病毒效价提高1000倍。 CAR被证明是猪水泡病病毒(SVDV)的功能性受体,因为CHO-CAR细胞而不是CHO模拟转染的对照易受SVDV感染,产生子代SVDV,并发展了细胞病变作用。此外,SVDV感染可以被抗CAR的单克隆抗体(RmcB)特异性阻断。抗CD55 MAb也抑制了HeLa细胞的SVDV感染,这表明该病毒像某些CVB一样,除了CAR外,还可能与CD55(衰变促进因子)相互作用。最后,用可溶性CAR预处理CVB或SVDV可有效阻断HeLa细胞单层的病毒感染。版权所有2000学术出版社。

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