Korte-Sarfaty J, Pham V D, Yant S, Hirano A, Wong T C
Department of Microbiology, University of Washington School of Medicine, Seattle, Washington, 98195, USA.
Biochem Biophys Res Commun. 1998 Aug 19;249(2):432-7. doi: 10.1006/bbrc.1998.9173.
Measles virus (MV) can infect mouse macrophages to cause a prolonged non-cytopathic infection that produces low levels of infectious virus for days. We have generated RAW264.7 mouse macrophages expressing human CD46, a cell surface complement regulatory protein that serves as a receptor for laboratory-adapted strains of MV. Laboratory-adapted MV strains efficiently enter the CD46-positive mouse macrophages to cause a cytopathic infection with extensive multinucleated cells and pseudopodia-like extensions. However, MV infection of mouse macrophages through CD46 is self-limiting. Both viral protein synthesis and infectious virus production are abruptly terminated after the second day of infection. This novel virus-cell interaction is seen only in mouse macrophages but not in mouse or hamster fibroblasts expressing human CD46. The possible role of CD46 in macrophage antiviral response restricting MV replication is discussed.
麻疹病毒（MV）可感染小鼠巨噬细胞，引发持续的非细胞病变性感染，数天内产生低水平的传染性病毒。我们构建了表达人CD46的RAW264.7小鼠巨噬细胞，人CD46是一种细胞表面补体调节蛋白，可作为实验室适应株MV的受体。实验室适应的MV株可有效进入CD46阳性小鼠巨噬细胞，引发细胞病变性感染，形成大量多核细胞和伪足样延伸。然而，通过CD46感染小鼠巨噬细胞的MV具有自我限制性。感染第二天后，病毒蛋白合成和传染性病毒产生均突然终止。这种新型病毒 - 细胞相互作用仅在小鼠巨噬细胞中出现，在表达人CD46的小鼠或仓鼠成纤维细胞中未观察到。本文讨论了CD46在巨噬细胞抗病毒反应中限制MV复制的可能作用。
