共 162 条
Retrovirus budding
被引:517
作者:

Morita, E
论文数: 0 引用数: 0
h-index: 0
机构:
Univ Utah, Dept Biochem, Salt Lake City, UT 84132 USA Univ Utah, Dept Biochem, Salt Lake City, UT 84132 USA

Sundquist, WI
论文数: 0 引用数: 0
h-index: 0
机构:
Univ Utah, Dept Biochem, Salt Lake City, UT 84132 USA Univ Utah, Dept Biochem, Salt Lake City, UT 84132 USA
机构:
[1] Univ Utah, Dept Biochem, Salt Lake City, UT 84132 USA
基金:
美国国家卫生研究院;
关键词:
HIV;
late domains;
multivesicular body;
Class E proteins;
virological synapse;
D O I:
10.1146/annurev.cellbio.20.010403.102350
中图分类号:
Q2 [细胞生物学];
学科分类号:
071009 ;
090102 ;
摘要:
Human immunodeficiency virus (HIV) and other retroviruses acquire their envelopes and spread infection by budding through the limiting membranes of producer cells. To facilitate budding, retroviruses usurp a cellular pathway that is normally used to create vesicles that bud into late endosomal compartments called multivesicular bodies (MVB). Research on yeast and human MVB biogenesis has led to the identification of similar to 25 human proteins that are required for vesicle formation and for HIV-1 budding, and has produced a working model for sequential recruitment of these proteins during MVB vesicle formation. Retroviruses can redirect this machinery to the plasma membrane and leave the cell in a single step or, alternatively, can bud directly into MVB compartments and then exit cells via the exosome pathway. Remarkably, virus release from both the plasma membrane and MVB compartments can occur directionally into specialized sites of cell-to-cell contact called virological synapses. Thus retroviruses have evolved elaborate mechanisms for escaping the cell and maximizing their chances of infecting a new host.
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页码:395 / 425
页数:31
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