Multiple isoforms of CD46 (membrane cofactor protein) serve as receptors for measles virus.

Multiple isoforms of CD46 (membrane cofactor protein) serve as receptors for measles virus.
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CD46(膜辅因子蛋白)的多种亚型可作为麻疹病毒的受体。

DOI:
10.1073/pnas.91.6.2161
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发表时间:
1994
影响因子:
11.1
通讯作者:
Oldstone,MB
Oldstone,MB
中科院分区:
综合性期刊1区
文献类型:
--
作者:
Manchester,M;Liszewski,MK;Atkinson,JP;Oldstone,MB

文献摘要

被引文献

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麻疹病毒(MV)在人类和某些猿宿主中引起生产性感染。啮齿动物细胞如中国仓鼠卵巢(CHO)和鼠细胞系通常抵抗MV感染。人CD 46,或膜辅因子蛋白,一种补体调节蛋白,最近已被报道为MV的细胞受体。CD 46蛋白存在多种亚型;其中四种亚型通常在人类细胞上表达。在CHO细胞中表达四种亚型中的每一种,然后暴露于MV,导致细胞内和细胞表面出现病毒蛋白,如通过免疫荧光检测到的。在培养物中也观察到合胞体形成。当接种在Vero细胞单层上时,表达四种亚型中任一种并暴露于MV的CHO细胞形成感染中心,表明细胞可将病毒传播给未感染的细胞。表达CD 46的BC 1同种型的鼠细胞系MC 57也对MV抗原染色呈阳性,并且在暴露于MV后在感染中心测定中呈阳性。用抗人CD 46抗体处理表达CD 46的细胞以剂量依赖性方式抑制MV结合。这些观察结果表明,CD 46的四种主要同种型中的任何一种都能够作为MV的受体。
Measles virus (MV) causes a productive infection in humans and certain simian hosts. Rodent cells such as Chinese hamster ovary (CHO) and murine cell lines normally resist MV infection. Human CD46, or membrane cofactor protein, a complement regulatory protein, recently has been reported as the cellular receptor for MV. Multiple isoforms of the CD46 protein exist; four of these isoforms are commonly expressed on human cells. Expression of each of the four isoforms in CHO cells followed by exposure to MV led to the appearance of viral proteins within the cells and on the cell surface as detected by immunofluorescence. Syncytium formation also was observed in the cultures. CHO cells expressing any of the four isoforms and exposed to MV formed infectious centers when plated on Vero cell monolayers, indicating that the cells can transmit virus to uninfected cells. The murine cell line MC57 expressing the BC1 isoform of CD46 also stained positively for MV antigens and was positive in the infectious center assay after exposure to MV. Treatment of CD46-expressing cells with antibody to human CD46 inhibited MV binding in a dose-dependent manner. These observations indicate that any of the four primary isoforms of CD46 are able to serve as a receptor for MV.