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人类内源性逆转录病毒K(HML-2)具有广泛的包膜介导的细胞嗜性,并且在进入后、整合前步骤易于受到抑制。

The human endogenous retrovirus K(HML-2) has a broad envelope-mediated cellular tropism and is prone to inhibition at a post-entry, pre-integration step.

作者信息

Kramer Philipp, Lausch Veronika, Volkwein Alexander, Hanke Kirsten, Hohn Oliver, Bannert Norbert

机构信息

Robert Koch Institute, Division for HIV and Other Retroviruses, Nordufer 20, 13353 Berlin, Germany.

Robert Koch Institute, Division for HIV and Other Retroviruses, Nordufer 20, 13353 Berlin, Germany.

出版信息

Virology. 2016 Jan;487:121-8. doi: 10.1016/j.virol.2015.10.014. Epub 2015 Oct 27.

DOI:10.1016/j.virol.2015.10.014
PMID:26517399
Abstract

The HERV-K(HML-2) family is the most recent addition to the collection of human endogenous retroviruses. It comprises proviruses that encode functional proteins that can assemble into replication defective particles carrying the envelope protein. Using a reconstituted HERV-K113 envelope sequence, we have analyzed its ability to mediate entry into a set of 33 cell lines from 10 species. Of these, 30 were permissive, demonstrating an amphotropism consistent with a broad expression of receptor protein(s). In an initial effort to identify a receptor for HERV-K(HML-2) we investigated whether transferrin receptor 1 and hyaluronidase 2, known cellular receptors of the closely related betaretroviruses mouse mammary tumor virus (MMTV) and Jaagsiekte sheep retrovirus (JSRV), could facilitate HERV-K(HML-2) entry. However, neither of these proteins could serve as a receptor for HERV-K(HML-2). Moreover, during attempts to further characterize the tropism of HERV-K(HML-2), we identified a cellular activity that inhibits infection at a post-entry, pre-integration step.

摘要

人内源性逆转录病毒K(HERV-K,HML-2)家族是人类内源性逆转录病毒集合中最新添加的成员。它包含一些前病毒,这些前病毒编码的功能蛋白能够组装成携带包膜蛋白的复制缺陷型颗粒。利用重组的HERV-K113包膜序列,我们分析了其介导进入来自10个物种的33种细胞系的能力。其中,30种细胞系具有易感性,显示出与受体蛋白广泛表达相一致的嗜性。在初步尝试鉴定HERV-K(HML-2)的受体时,我们研究了转铁蛋白受体1和透明质酸酶2(密切相关的β逆转录病毒小鼠乳腺肿瘤病毒(MMTV)和绵羊肺腺瘤病毒(JSRV)已知的细胞受体)是否能促进HERV-K(HML-2)的进入。然而,这两种蛋白都不能作为HERV-K(HML-2)的受体。此外,在进一步表征HERV-K(HML-2)嗜性的尝试过程中,我们鉴定出一种在病毒进入后、整合前步骤抑制感染的细胞活性。

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