The potential role of microfilaments in host cells for infection with infectious spleen and kidney necrosis virus infection

Virology Journal

Jian-guo He²  Shao-ping Weng²  Xiao-Dong Li²  Shu Mi²  Qiong Xia²  Chang-jun Guo¹  Zhao-yu Liu²  Kun-tong Jia² 

[1] MOE Key Laboratory of Aquatic Product Safety/State Key Laboratory for Biocontrol, School of Marine Sciences, Sun Yat-sen University, 135 Xingang Road West, Guangzhou, 510275, PR China;State Key Laboratory for Biocontrol, School of Life Sciences, Sun Yat-sen University, 135 Xingang Road West, Guangzhou, 510275, PR China

关键词: Microfilaments;    Infectious spleen and kidney necrosis virus;    Iridovirus;   

Others  :  1151341
DOI  :  10.1186/1743-422X-10-77

 received in 2012-07-25, accepted in 2013-02-27,  发布年份 2013

【 摘 要 】

Background

Infectious spleen and kidney necrosis virus (ISKNV) belongs to the genus Megalocytivirus from the family Iridoviridae. Megalocytivirus causes severe economic losses to tropical freshwater and marine culture industry in Asian countries and is devastating to the mandarin fish farm industry in China particularly.

Methods

We investigated the involvement of microfilaments in the early and late stages of ISKNV infection in MFF-1 cells by selectively perturbing their architecture using well-characterized inhibitors of actin dynamics. The effect of disruption of actin cytoskeleton on ISKNV infection was evaluated by indirect immunofluorescence analysis or real-time quantitative PCR.

Results

The depolymerization of the actin filaments with cytochalasin D, cytochalasin B, or latrunculin A reduced ISKNV infection. Furthermore, depolymerization of filamentous actin by inhibitors did not inhibit binding of the virus but affected virus internalization in the early stages of infection. In addition, the depolymerization of actin filaments reduced total ISKNV production in the late stages of ISKNV.

Conclusions

This study demonstrated that ISKNV required an intact actin network during infection. The findings will help us to better understand how iridoviruses exploit the cytoskeleton to facilitate their infection and subsequent disease.

【 授权许可】

   
2013 Jia et al; licensee BioMed Central Ltd.

【 图 表 】

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