title: Cofilin 1-mediated biphasic F-actin dynamics of neuronal cells affect herpes simplex virus 1 infection and replication.
abstract: Herpes simplex virus 1 (HSV-1) invades the nervous system and causes pathological changes. In this study, we defined the remodeling of F-actin and its possible mechanisms during HSV-1 infection of neuronal cells. HSV-1 infection enhanced the formation of F-actin-based structures in the early stage of infection, which was followed by a continuous decrease in F-actin during the later stages of infection. The disruption of F-actin dynamics by chemical inhibitors significantly reduced the efficiency of viral infection and intracellular HSV-1 replication. The active form of the actin-depolymerizing factor cofilin 1 was found to increase at an early stage of infection and then to continuously decrease in a manner that corresponded to the remodeling pattern of F-actin, suggesting that cofilin 1 may be involved in the biphasic F-actin dynamics induced by HSV-1 infection. Knockdown of cofilin 1 impaired HSV-1-induced F-actin assembly during early infection and inhibited viral entry; however, overexpression of cofilin 1 did not affect F-actin assembly or viral entry during early infection but decreased intracellular viral reproduction efficiently. Our results, for the first time, demonstrated the biphasic F-actin dynamics in HSV-1 neuronal infection and confirmed the association of F-actin with the changes in the expression and activity of cofilin 1. These results may provide insight into the mechanism by which HSV-1 productively infects neuronal cells and causes pathogenesis.
authors.affiliation: Guangdong Provincial Key Laboratory of Bioengineering Medicine, National Engineering Research Center of Genetic Medicine, Jinan University, Guangzhou, China.
authors.forename: Yangfei
authors.initials: Y
authors.lastname: Xiang
authors.forename: Kai
authors.initials: K
authors.lastname: Zheng
authors.forename: Huaiqiang
authors.initials: H
authors.lastname: Ju
authors.forename: Shaoxiang
authors.initials: S
authors.lastname: Wang
authors.forename: Ying
authors.initials: Y
authors.lastname: Pei
authors.forename: Weichao
authors.initials: W
authors.lastname: Ding
authors.forename: Zhenping
authors.initials: Z
authors.lastname: Chen
authors.forename: Qiaoli
authors.initials: Q
authors.lastname: Wang
authors.forename: Xianxiu
authors.initials: X
authors.lastname: Qiu
authors.forename: Meigong
authors.initials: M
authors.lastname: Zhong
authors.forename: Fanli
authors.initials: F
authors.lastname: Zeng
authors.forename: Zhe
authors.initials: Z
authors.lastname: Ren
authors.forename: Chuiwen
authors.initials: C
authors.lastname: Qian
authors.forename: Ge
authors.initials: G
authors.lastname: Liu
authors.forename: Kaio
authors.initials: K
authors.lastname: Kitazato
authors.forename: Yifei
authors.initials: Y
authors.lastname: Wang
mesh_terms: D000199:Actins / Q000378:metabolism*; D002460:Cell Line; D051338:Cofilin 1 / Q000378:metabolism*; D018259:Herpesvirus 1, Human / Q000502:physiology*; D006801:Humans; D009474:Neurons / Q000378:metabolism* / Q000821:virology*; D053586:Virus Internalization; D014779:Virus Replication
chemical_list: D000199:Actins; D051338:Cofilin 1