ArticleVirus genes2014
ORF005L from infectious spleen and kidney necrosis virus is located in the inner mitochondrial membrane and induces apoptosis.
Article in Virus genes, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 11 citations in OpenAlex.
- Investigating the mechanism of heat-shock protection in ISKNV-infected tilapia brain cell line.Microbiology spectrum · 2025Article
- The mTOR/PGC-1α/SIRT3 Pathway Drives Reductive Glutamine Metabolism to Reduce Oxidative Stress Caused by ISKNV in CPB Cells.Microbiology spectrum · 2022Article
- pol-miR-731, a teleost miRNA upregulated by megalocytivirus, negatively regulates virus-induced type I interferon response, apoptosis, and cell cycle arrest.Scientific reports · 2016Article
- A mitochondrial outer membrane-localized protein encoded by White spot syndrome virus.Virus genes · 2016Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Infectious spleen and kidney necrosis virus (ISKNV) belongs to the genus Megalocytivirus in the family Iridoviridae. This virus is the etiological agent of a serious and pandemic disease in fish. Cells infected with ISKNV undergo apoptosis. In this study, the ISKNV ORF005L gene was characterized and functionally investigated. Bioinformatics analysis revealed that the ORF005L protein contains a region similar to the catalytic domain of CTD-like phosphatases. Real-time quantitative-PCR results showed the transcription profile of ORF005L in ISKNV-infected cells; in these cells, ORF005L was initially transcribed at 24 h post-infection. The green fluorescent protein-tagged ORF005L protein was localized in the mitochondria. Sub-mitochondrial fractions were subjected to Western blot, and the results showed that ORF005L was specifically located in the inner membrane of the mitochondria. The ORF005L in fathead minnow cells was transiently expressed, resulting in the decrease in mitochondrial transmembrane potential, which induced cell apoptosis. ORF005L was knocked down by specific dsRNA, thereby significantly reducing the apoptosis of mandarin fish fry-1 cells induced by ISKNV infection. These results indicated that the ORF005L of ISKNV could disrupt mitochondrial function and cause apoptosis. This study may provide novel insights into the pathogenesis of Megalocytivirus infection.
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