Wudiri George A, Pritchard Suzanne M, Li Hong, Liu Jin, Aguilar Hector C, Gilk Stacey D, Nicola Anthony V
Department of Veterinary Microbiology and Pathology, Washington State University, Pullman, Washington, USA Paul G. Allen School for Global Animal Health, Washington State University, Pullman, Washington, USA.
Department of Veterinary Microbiology and Pathology, Washington State University, Pullman, Washington, USA.
J Virol. 2014 Dec;88(23):13918-22. doi: 10.1128/JVI.01615-14. Epub 2014 Sep 17.
Herpes simplex virus 1 (HSV-1) required cholesterol or desmosterol for virion-induced membrane fusion. HSV successfully entered DHCR24(-/-) cells, which lack a desmosterol-to-cholesterol conversion enzyme, indicating that entry can occur independently of cholesterol. Depletion of desmosterol from these cells resulted in diminished HSV-1 entry, suggesting a general sterol requirement for HSV-1 entry and that desmosterol can operate in virus entry. Cholesterol functioned more effectively than desmosterol, suggesting that the hydrocarbon tail of cholesterol influences viral entry.
单纯疱疹病毒1型(HSV-1)的病毒体诱导膜融合需要胆固醇或羊毛甾醇。HSV成功进入缺乏羊毛甾醇向胆固醇转化酶的DHCR24(-/-)细胞,这表明病毒进入可独立于胆固醇发生。从这些细胞中去除羊毛甾醇会导致HSV-1进入减少,这表明HSV-1进入普遍需要甾醇,且羊毛甾醇可在病毒进入过程中发挥作用。胆固醇比羊毛甾醇的作用更有效,这表明胆固醇的烃链影响病毒进入。