病毒进入。拉沙病毒进入需要触发诱导的受体开关。
Virus entry. Lassa virus entry requires a trigger-induced receptor switch.
机构信息
Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX, Amsterdam, Netherlands.
Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX, Amsterdam, Netherlands. Department of Microbiology and Immunobiology, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA.
出版信息
Science. 2014 Jun 27;344(6191):1506-10. doi: 10.1126/science.1252480.
Lassa virus spreads from a rodent to humans and can lead to lethal hemorrhagic fever. Despite its broad tropism, chicken cells were reported 30 years ago to resist infection. We found that Lassa virus readily engaged its cell-surface receptor α-dystroglycan in avian cells, but virus entry in susceptible species involved a pH-dependent switch to an intracellular receptor, the lysosome-resident protein LAMP1. Iterative haploid screens revealed that the sialyltransferase ST3GAL4 was required for the interaction of the virus glycoprotein with LAMP1. A single glycosylated residue in LAMP1, present in susceptible species but absent in birds, was essential for interaction with the Lassa virus envelope protein and subsequent infection. The resistance of Lamp1-deficient mice to Lassa virus highlights the relevance of this receptor switch in vivo.
拉沙病毒可在鼠类与人之间传播，并可导致致命性出血热。尽管拉沙病毒具有广泛的嗜性，但 30 年前有报道称鸡细胞能抵抗感染。我们发现拉沙病毒在禽类细胞中能轻易地与细胞表面受体α- 肌动蛋白结合，但在易感物种中，病毒进入需要依赖 pH 值的细胞内受体——溶酶体驻留蛋白 LAMP1。反复的单倍体筛选揭示，唾液酸转移酶 ST3GAL4 对于病毒糖蛋白与 LAMP1 的相互作用是必需的。LAMP1 上存在一个糖基化残基，仅在易感物种中存在而在鸟类中缺失，对于与拉沙病毒包膜蛋白的相互作用以及随后的感染是必需的。Lamp1 缺陷型小鼠对拉沙病毒的抗性突出了该受体转换在体内的相关性。
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