Yellow fever 17D virus: pseudo-revertant suppression of defective virus penetration and spread by mutations in domains II and III of the E protein.
Yellow fever 17D virus: pseudo-revertant suppression of defective virus penetration and spread by mutations in domains II and III of the E protein.
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黄热病 17D 病毒：通过 E 蛋白结构域 II 和 III 的突变，对有缺陷的病毒渗透和传播进行假回复抑制。
DOI：
10.1016/j.virol.2004.06.015
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发表时间：
2004
期刊：
影响因子：
--
通讯作者：
Chambers,ThomasJ
中科院分区：
文献类型：
--
作者：
Vlaycheva,Leonssia;Nickells,Michael;Droll,DeborahA;Chambers,ThomasJ
A yellow fever (YFV) 17D virus variant, which causes persistent infection of mouse neuroblastoma cells associated with defective cell penetration and small plaque size, yielded plaque-revertant viruses from cells transfected with viral transcripts encoding the adaptive mutation (Gly360in the E protein). Reconstruction of a plaque-purified revertant which contained Gly360and additional substitutions (Asn for Lys303and Val for Ala261) yielded a virus whose infectious center size, growth efficiency, and cell penetration rate similar to the parental YF5.2iv virus, whereas viruses with Asn303or Val261alone with Gly360yielded either a small-plaque virus or a parental revertant. These data indicate that the YFV E protein is subject to suppression of mutations in domain III that are deleterious for viral entry and spread by a second-site mutation in domain II. Position 261 lies within the hydrophobic ligand-binding pocket at the domain I–II interface, a site believed to be involved in the hinge-like conformational change of domain II during activation of membrane fusion-activity. Results of this study provide genetic data consistent with findings on flavivirus structure and implicate domain III in functions beyond simply cell surface attachment.
黄热病病毒法国神经性疫苗株与猴脑的相互作用：猴脑膜受体逃逸变体的表征
影响因子：
5.4
作者：
H. Ni;K. Ryman;Heiman Wang;M. Saeed;R. Hull;D. Wood;P. Minor;S. Watowich;A. Barrett
通讯作者：
A. Barrett
影响因子：
3.7
作者：
Ryman, KD;Ledger, TN;Barrett, ADT
通讯作者：
Barrett, ADT