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Journal Article

Disease resistance and immune‐relevant gene expression in golden mandarin fish, Siniperca scherzeri Steindachner, infected with infectious spleen and kidney necrosis virus‐like agent

G W Shin; S L White; H U Dahms; H D Jeong; J H Kim
Journal of Fish Diseases · Vol. 37, Issue 12 · pp. 1041-1054 · 2014

Abstract

Infectious spleen and kidney necrosis virus (ISKNV), family Iridoviridae , genus Megalocytivirus, may cause high mortality rates such as those seen in mandarin fish, Siniperca chuatsi . ISKNV has attracted much attention due to the possible environmental threat and economic losses it poses on both cultured and wild populations. We have investigated the pathogenicity of ISKNV‐like agent Megalocytivirus , isolated from infected pearl gourami, in golden mandarin fish, Siniperca scherzeri – a member of the Percichthyidae family – and in another Percichthyidae species, S. chuatsi . Fish were challenged with four different doses of ISKNV‐like agent Megalocytivirus (1, 10, 100 or 1000 μg per fish) over a 30‐day period, and cumulative fish mortalities were calculated for each group. No significant mortality was observed for fish challenged with the lowest dose (1 μg per fish) relative to a control group. However, all other challenged groups showed 100% mortality over a 30‐day period in proportion to the challenge dose. Quantitative real‐time PCR was performed to measure mRNA expression levels for six immune‐related genes in golden mandarin fish following ISKNV‐like agent challenge. mRNA expression levels for IRF1, Mx, viperin and interleukin 8 significantly increased, while mRNA levels for IRF2 and IRF7 remained constant or declined during the challenge period.

Bibliographic Information

JournalJournal of Fish Diseases
PublisherWiley
Publication Date2014-12-01
Publication Year2014
Volume37
Issue12
Pages1041-1054
Document TypeJournal Article
Print ISSN0140-7775
eISSN1365-2761
DOI10.1111/jfd.12182
SubjectGeneral Aquaculture, Fisheries & Fish Science

Access Information

NARA Access Coverage1997-01-01~Current
Journal Homepagehttps://onlinelibrary.wiley.com/loi/13652761
Publisher PageOpen Publisher Page
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