Mebatsion T, Konig M, Conzelmann K K
Institute of Clinical Virology, Federal Research Centre for Virus Diseases of Animals, Tübingen, Federal Republic of Germany.
Cell. 1996 Mar 22;84(6):941-51. doi: 10.1016/s0092-8674(00)81072-7.
Budding of enveloped viruses from cellular membranes is believed to de pend on the presence of transmembrane spike proteins interacting with cytoplasmic virus components. To address the mechanism of rhabdovirus budding, we generated rabies virus mutants deficient for the glycoprotein G or the G cytoplasmic tail. We found that spikeless rhabdovirus particles were released from cells infected with the G-deficient mutant, demonstrating that a viral surface protein is not required to drive the budding process. However, particle production is enhanced approximately 6-fold and 30-fold in the presence of tailless G or G, respectively. This reveals that G also possesses an intrinsic and independent exocytosis activity. We propose a model according to which efficient budding of rhabdoviruses is achieved by a concerted action of both core and spike proteins.
包膜病毒从细胞膜出芽被认为依赖于跨膜刺突蛋白与细胞质病毒成分的相互作用。为了研究弹状病毒出芽的机制，我们构建了缺乏糖蛋白G或G细胞质尾巴的狂犬病病毒突变体。我们发现，无刺突的弹状病毒颗粒从感染了G缺陷突变体的细胞中释放出来，这表明驱动出芽过程不需要病毒表面蛋白。然而，分别在无尾G或G存在的情况下，颗粒产生量分别增加了约6倍和30倍。这表明G也具有内在且独立的胞吐活性。我们提出了一个模型，根据该模型，弹状病毒的有效出芽是通过核心蛋白和刺突蛋白的协同作用实现的。
