Abstract
BackgroundInfectious 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.MethodsWe 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.ResultsThe 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.ConclusionsThis 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.
Highlights
Infectious spleen and kidney necrosis virus (ISKNV) belongs to the genus Megalocytivirus from the family Iridoviridae
We have previously demonstrated that ISKNV enters mandarin fish fry 1 (MFF-1) cells through a caveola-mediated internalization mechanism, and the microtubules of MFF-1 cells may play a role in the entry of ISKNV [19]
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 pharmacological agents
Summary
Infectious spleen and kidney necrosis virus (ISKNV) belongs to the genus Megalocytivirus from the family Iridoviridae. Intracellular pathogens are well known to use and manipulate cellular machinery to accomplish their life cycle. The infection cycle of animal viruses can be divided into three essential steps: entry into a host cell, replication, and egression to infect another cell. The restrictions of free diffusion in the cytoplasm and the limited coding capacity of viruses force them to manipulate cellular metabolic pathways to achieve each of these steps [1]. Most viruses utilize the cytoskeleton, including actin microfilaments (F-actin) and microtubules, for various stages of their life cycle. Numerous viral proteins have been reported to interact with actin-binding proteins or directly with actin, such as the baculovirus VP80 protein [10], the NS3 and NS5A proteins (where NS indicates non-structural) of hepatitis C virus [11], the NS1 protein of influenza A [12], and Gag of equine infectious anemia virus [13]
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