Mechanisms of enveloped virus entry into animal cells

Klasse, Per Johan; Bron, Romke; Marsh, Mark

doi:10.1016/s0169-409x(98)00002-7

Cited by 79 publications

(61 citation statements)

References 256 publications

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“…To initiate infection, influenza viruses release their genome into the cytoplasm by fusing with endosomes 1,9,[18][19][20][21][22][23] . We tested whether the clathrin-mediated pathway and clathrin-and caveolin-independent pathway both lead to viral fusion.…”

Section: Clathrin-and Caveolin-independent Pathwaymentioning

confidence: 99%

Assembly of endocytic machinery around individual influenza viruses during viral entry

Rust

Lakadamyali

Zhang

et al. 2004

Nat Struct Mol Biol

415

421

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Most viruses enter cells via receptor-mediated endocytosis. However, the entry mechanisms used by many of them remain unclear. How viruses are targeted to cellular endocytic machinery is also largely unknown. We have studied the entry mechanisms of influenza viruses by tracking the interaction of single viruses with cellular endocytic structures in real time using fluorescence microscopy. Our results show that influenza can exploit clathrin-mediated and clathrin-and caveolin-independent endocytic pathways in parallel, both pathways leading to viral fusion with similar efficiency. Remarkably, viruses taking the clathrin-mediated pathway enter cells via the de novo formation of clathrin-coated pits (CCPs) at viral binding sites. CCP formation at these sites is much faster than elsewhere on the cell surface, suggesting a virus-induced CCP formation mechanism that may be commonly exploited by many other types of viruses.

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Section: Clathrin-and Caveolin-independent Pathwaymentioning

confidence: 99%

Assembly of endocytic machinery around individual influenza viruses during viral entry

Rust

Lakadamyali

Zhang

et al. 2004

Nat Struct Mol Biol

415

421

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“…Viral entry mechanisms are commonly multistep processes, and many viruses use two or more proteins in concert to achieve cell entry (35,36). In BTV, VP2 protein has been shown to be responsible for receptor binding and has the viral hemagglutination activity (26).…”

Section: Is the Fusion Activity Of Vp5 Influenced By The Btv Receptormentioning

confidence: 99%

A capsid protein of nonenveloped Bluetongue virus exhibits membrane fusion activity

Forzan

Wirblich

Roy

2004

Proc. Natl. Acad. Sci. U.S.A.

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The outer capsid layer of Bluetongue virus, a member of the nonenveloped Reoviridae family, is composed of two proteins, a receptor-binding protein, VP2, and a second protein, VP5, which shares structural features with class I fusion proteins of enveloped viruses. In the replication cycle of Bluetongue virus VP5 acts as a membrane permeabilization protein that mediates release of viral particles from endosomal compartments into the cytoplasm. Here, we show that VP5 can also act as a fusion protein and induce syncytium formation when it is fused to a transmembrane anchor and expressed on the cell surface. Fusion activity is strictly pHdependent and is triggered by short exposure to low pH. No cell-cell fusion is observed at neutral pH. Deletion of the first 40 amino acids, which can fold into two amphipathic helices, abolishes fusion activity. Syncytium formation by VP5 is inhibited in the presence of VP2 when it is expressed in a membrane-anchored form. The data indicate an interaction between the outer capsid protein VP2 and VP5 and show that VP5 undergoes pH-dependent conformational changes that render it capable of interacting with cellular membranes. More importantly, our data show that a membrane permeabilization protein of a nonenveloped virus can evolve into a fusion protein by the addition of an appropriate transmembrane anchor. The results strongly suggest that the mechanism of membrane permeabilization by VP5 and membrane fusion by viral fusion proteins require similar structural features and conformational changes.

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“…The endocytosed viruses are internalized through endocytic compartments, and the viruses fuse with the endosomal membrane to release viral genome into host cells. [20][21][22][23] During these processes, viruses utilize microtubule networks for movement toward the perinuclear regions. 24,25 Recent studies have shown that intracellular virus trafficking is critically involved in the endosomemediated sorting and transport of influenza virus, vesicular stomatitis virus (VSV) and Semliki Forest virus.…”

Section: Introductionmentioning

confidence: 99%