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  4. Transcriptional analysis of orange-spotted grouper reacting to experimental grouper iridovirus infection
 
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Transcriptional analysis of orange-spotted grouper reacting to experimental grouper iridovirus infection

Resource
DEVELOPMENTAL AND COMPARATIVE IMMUNOLOGY, 37(2), 233-242
Journal
Developmental & Comparative Immunology
Pages
233-242
Date Issued
2012
Date
2012
Author(s)
Wu, Ming-Shan
Chen, Chien-Wen
Liu, Yu-Cheng
Huang, Hseng-Hsiang
Lin, Chih-Hung
Tzeng, Chyng-Shyan
Chang, Chi-Yao
DOI
10.1016/j.dci.2012.04.002
URI
http://ntur.lib.ntu.edu.tw//handle/246246/243408
Abstract
Disease caused by grouper iridovirus (GIV) has resulted in economic losses due to high mortality in grouper culture. Thirty-eight up- and 48 down-regulated known entities have been identified using a GIV-infected grouper kidney cDNA microarray chip. Further quantitative validation was executed in the head-kidney and spleen for 24 candidate genes and 7 immune factors following GIV inoculation. Significant induction with various patterns could be seen in 30 tested genes in the spleen. However, only 23 genes had induction in the head-kidney and meanwhile 5 genes showed reduction. Transcriptional expression profiles of selected genes in response to lipopolysaccharide (LPS) or polyinosinic:polycytidylic acid (PIC) were also established to compare with the GIV-stimulated expression. The results indicated that the responses of most genes facing GIV invasion have more similarities to PIC treatment than LPS. Seven genes are thought to be interferon-related factors: RNA helicase DHX58, ISG15, viperin, HECT E3 ligase (HECT), CD9, urokinase plasminogen activator surface receptor (PLAUR) and Mx-1. Following immunization with inactivated GIV, significant induction could be seen in DHX58, viperin, IL-1β, IL-8, COX-2, HECT, PLAUR, IgM, Mx-1, very large inducible GTPase-1 (VLIG1) and TNF-α in the head-kidney or spleen, and the latter 6 genes also had a gradual increasing pattern by a boosting immunization. These factors might play important roles in adaptive antiviral protection. Thus, we have characterized the temporal response patterns of virus responsive genes and have also identified several potential immune markers to further investigate host antiviral defense mechanisms. © 2012 Elsevier Ltd.
Subjects
Grouper; Immunization; Iridovirus; Microarray; Quantitative PCR
SDGs

[SDGs]SDG14

Other Subjects
CD9 antigen; complementary DNA; cyclooxygenase 2; immunoglobulin M; interleukin 1beta; interleukin 8; lipopolysaccharide; polyinosinic polycytidylic acid; tumor necrosis factor alpha; urokinase receptor; animal experiment; animal tissue; article; CD9 gene; controlled study; cyclooxygenase 2 gene; DNA microarray; DNA virus infection; down regulation; Epinephelus coioides; gene expression profiling; gene expression regulation; gene function; gene induction; genetic analysis; genetic selection; genetic similarity; head; HECT E3 ubiquitin ligase gene; immune response gene; immunoglobulin M gene; interferon stimulated gene 15 gene; interleukin 1beta gene; interleukin 8 gene; Iridovirus; Iridovirus infection; kidney parenchyma; marine species; Mx 1 gene; nonhuman; nucleotide sequence; priority journal; RNA helicase DHX58 gene; spleen; transcription regulation; tumor necrosis factor alpha gene; unindexed sequence; urokinase plasminogen activator surface receptor gene; very large inducible GTPase 1 gene; viperin gene; virus inactivation; virus virulence; Animals; DNA Virus Infections; Fish Diseases; Gene Expression Profiling; Head Kidney; Perciformes; Ranavirus; Epinephelinae; Epinephelus coioides; Great Island virus; Grouper iridovirus; Iridovirus
Type
journal article
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