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The potential role of microfilaments in host cells for infection with infectious spleen and kidney necrosis virus infection
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...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3599308/ https://www.ncbi.nlm.nih.gov/pubmed/23497248 http://dx.doi.org/10.1186/1743-422X-10-77 |
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author | Jia, Kun-tong Liu, Zhao-yu Guo, Chang-jun Xia, Qiong Mi, Shu Li, Xiao-Dong Weng, Shao-ping He, Jian-guo |
author_facet | Jia, Kun-tong Liu, Zhao-yu Guo, Chang-jun Xia, Qiong Mi, Shu Li, Xiao-Dong Weng, Shao-ping He, Jian-guo |
author_sort | Jia, Kun-tong |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-3599308 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-35993082013-03-17 The potential role of microfilaments in host cells for infection with infectious spleen and kidney necrosis virus infection Jia, Kun-tong Liu, Zhao-yu Guo, Chang-jun Xia, Qiong Mi, Shu Li, Xiao-Dong Weng, Shao-ping He, Jian-guo Virol J Research 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. BioMed Central 2013-03-07 /pmc/articles/PMC3599308/ /pubmed/23497248 http://dx.doi.org/10.1186/1743-422X-10-77 Text en Copyright ©2013 Jia et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Jia, Kun-tong Liu, Zhao-yu Guo, Chang-jun Xia, Qiong Mi, Shu Li, Xiao-Dong Weng, Shao-ping He, Jian-guo The potential role of microfilaments in host cells for infection with infectious spleen and kidney necrosis virus infection |
title | The potential role of microfilaments in host cells for infection with infectious spleen and kidney necrosis virus infection |
title_full | The potential role of microfilaments in host cells for infection with infectious spleen and kidney necrosis virus infection |
title_fullStr | The potential role of microfilaments in host cells for infection with infectious spleen and kidney necrosis virus infection |
title_full_unstemmed | The potential role of microfilaments in host cells for infection with infectious spleen and kidney necrosis virus infection |
title_short | The potential role of microfilaments in host cells for infection with infectious spleen and kidney necrosis virus infection |
title_sort | potential role of microfilaments in host cells for infection with infectious spleen and kidney necrosis virus infection |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3599308/ https://www.ncbi.nlm.nih.gov/pubmed/23497248 http://dx.doi.org/10.1186/1743-422X-10-77 |
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