Schneider-Schaulies Sibylle, Schneider-Schaulies Jürgen, Niewiesk Stefan, Ter Meulen Volker
Institute for Virology and Immunobiology, University of Würzburg, Versbacher Str. 7, Germany.
Med Microbiol Immunol. 2002 Oct;191(2):83-7. doi: 10.1007/s00430-002-0121-6. Epub 2002 Aug 17.
As important determinants of measles virus (MV) pathogenicity, the MV glycoproteins play a key role in conferring the cellular tropism of this virus, but also in modulating the activity of immunocompetent cells. Whereas all MV strains are able to use CD150 (SLAM) for binding and entry into target cells, only certain, mainly vaccine, strains, can use both CD46 and CD150. Both molecules are down-regulated from the cell surface and this is brought about by both infection and contact with the MV H protein of strains that are able to interact with these molecules. Whereas down-regulation of CD46 could be linked to enhanced sensitivity to complement-mediated lysis, and may thus represent an attenuation marker for vaccine strains, pathogenetic consequences of CD150 down-regulation are unknown as yet. Although the role of CD150 is not entirely clear, viruses containing a wild-type strain-derived H protein revealed a particular tropism for human dendritic cells in vitro, and replicated well in secondary lymphatic tissues of cotton rats where they were also able to cause immunosuppression, as documented by an impaired proliferative response of lymphocytes ex vivo. Most likely, inhibition of T cell expansion by these cells is brought about by another activity of the MV glycoprotein complex, namely by disrupting a pathway important for S-phase entry of T cells, by a mere surface contact.
作为麻疹病毒（MV）致病性的重要决定因素，MV糖蛋白在赋予该病毒细胞嗜性方面发挥关键作用，同时也在调节免疫活性细胞的活性方面发挥作用。所有MV毒株都能够利用CD150（信号淋巴细胞激活分子）结合并进入靶细胞，而只有某些毒株（主要是疫苗毒株）能够同时利用CD46和CD150。这两种分子都会从细胞表面下调，这是由感染以及与能够与这些分子相互作用的毒株的MV H蛋白接触所导致的。虽然CD46的下调可能与对补体介导的裂解的敏感性增强有关，因此可能代表疫苗毒株的减毒标记，但CD150下调的致病后果尚不清楚。虽然CD150的作用尚不完全清楚，但含有野生型毒株来源的H蛋白的病毒在体外对人树突状细胞显示出特定的嗜性，并且在棉鼠的二级淋巴组织中复制良好，在那里它们也能够引起免疫抑制，如体外淋巴细胞增殖反应受损所证明的那样。很可能，这些细胞对T细胞扩增的抑制是由MV糖蛋白复合物的另一种活性引起的，即通过单纯的表面接触破坏对T细胞进入S期很重要的一条途径。
