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The article explores the methylation of the genome of Infectious spleen and kidney necrosis virus (ISKNV), a fish iridovirus, and its role in viral infection. The methylation level of ISKNV is 23.44%, and it is essential for viral amplification. The study suggests that genome methylation levels may impact the immune response and pathogenicity of the virus. The research provides new insights into the role of genome methylation in viral infection.
Iridoviruses are nucleocytoplasmic large dsDNA viruses that infect invertebrates and ectothermic vertebrates. The hypermethylated genome of vertebrate iridoviruses is unique among animal viruses. However, the map and function of iridovirus genomic methylation remain unknown. Herein, the methylated genome of Infectious spleen and kidney necrosis virus (ISKNV, a fish iridovirus), and its role in viral infection, are investigated. The methylation level of ISKNV is 23.44%. The hypermethylated genome is essential for ISKNV amplification, but there is no correlation between hypermethylation and viral gene expression. The hypomethylated ISKNV (obtained via 5-Azacytidine) activates a strong immunoreaction in vitro and reduces its pathogenicity in vivo. The unmethylated viral DNA can induce a stronger immunoreaction in vitro, whereas inactivated hypomethylated ISKNV can induce a stronger immunoreaction in vivo, suggesting ISKNV may evade from immune system by increasing its genome methylation level. Our work provides new insights into the role of genome methylation in viral infection.
DNA methylation is an epigenetic mechanism involving the transfer of a methyl group onto the C5 position of cytosine to form 5-methylcytosine, thereby frequently inhibiting gene expression and modifying the function of genes1,<a data-track="click" data-track-action="reference anchor" data-track-label="link" data-test="citation-ref" aria-label="Reference 2" title="Laird, P. W. Principles and challenges of genome-wide DNA methylation