生物
萌芽
狂犬病病毒
病毒学
狂犬病
溶血酶
病毒
弹状病毒科
遗传学
作者
Atsushi Okumura,Ronald N. Harty
标识
DOI:10.1016/b978-0-12-387040-7.00002-0
摘要
Rabies virus (RABV) and other negative-strand RNA viruses are the causes of serious diseases in humans and animals worldwide. Assembly and budding are important late events in the replication cycles of these negative-strand RNA viruses that have received much attention in the past decade. Indeed, important insights into the molecular mechanisms by which rhabdoviral proteins usurp and/or interact with host proteins to promote efficient virion assembly and egress has greatly enhanced our understanding of the budding process. Assembly/budding of rhabdoviruses is driven largely by the matrix (M) protein. RABV M protein contains a late budding domain that mediates the recruitment of host proteins linked to the vacuolar protein sorting pathway of the cell to facilitate virus–cell separation. This chapter summarizes our current knowledge of the roles that both RABV M protein and interacting host proteins play during the budding process.
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