Scale Drop Disease Virus (SDDV) and Lates calcarifer Herpes Virus (LCHV) coinfection downregulate immune-relevant pathways and cause splenic and kidney necrosis in barramundi under commercial farming conditions

Domingos, Jose A., Shen, Xueyan, Terence, Celestine, Senapin, Saengchan, Dong, Ha Thanh, Tan, Marie R., Gibson-Kueh, Susan, and Jerry, Dean R. (2021) Scale Drop Disease Virus (SDDV) and Lates calcarifer Herpes Virus (LCHV) coinfection downregulate immune-relevant pathways and cause splenic and kidney necrosis in barramundi under commercial farming conditions. Frontiers in Genetics, 12. 666897.

PDF (Published Version) - Published Version
Available under License Creative Commons Attribution.

Download (1MB) | Preview
View at Publisher Website:


Marine farming of barramundi (Lates calcarifer) in Southeast Asia is currently severely affected by viral diseases. To better understand the biological implications and gene expression response of barramundi in commercial farming conditions during a disease outbreak, the presence of pathogens, comparative RNAseq, and histopathology targeting multiple organs of clinically “sick” and “healthy” juveniles were investigated. Coinfection of scale drop disease virus (SDDV) and L. calcarifer herpes virus (LCHV) were detected in all sampled fish, with higher SDDV viral loads in sick than in healthy fish. Histopathology showed that livers in sick fish often had moderate to severe abnormal fat accumulation (hepatic lipidosis), whereas the predominant pathology in the kidneys shows moderate to severe inflammation and glomerular necrosis. The spleen was the most severely affected organ, with sick fish presenting severe multifocal and coalescing necrosis. Principal component analysis (PC1 and PC2) explained 70.3% of the observed variance and strongly associated the above histopathological findings with SDDV loads and with the sick phenotypes, supporting a primary diagnosis of the fish being impacted by scale drop disease (SDD). Extracted RNA from kidney and spleen of the sick fish were also severely degraded likely due to severe inflammation and tissue necrosis, indicating failure of these organs in advanced stages of SDD. RNAseq of sick vs. healthy barramundi identified 2,810 and 556 differentially expressed genes (DEGs) in the liver and muscle, respectively. Eleven significantly enriched pathways (e.g., phagosome, cytokine-cytokine-receptor interaction, ECM-receptor interaction, neuroactive ligand-receptor interaction, calcium signaling, MAPK, CAMs, etc.) and gene families (e.g., tool-like receptor, TNF, lectin, complement, interleukin, chemokine, MHC, B and T cells, CD molecules, etc.) relevant to homeostasis and innate and adaptive immunity were mostly downregulated in sick fish. These DEGs and pathways, also previously identified in L. calcarifer as general immune responses to other pathogens and environmental stressors, suggest a failure of the clinically sick fish to cope and overcome the systemic inflammatory responses and tissue degeneration caused by SDD.

Item ID: 68542
Item Type: Article (Research - C1)
ISSN: 1664-8021
Copyright Information: Copyright © 2021 Domingos, Shen, Terence, Senapin, Dong, Tan, Gibson-Kueh and Jerry. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s)are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
Funders: Singapore Food Agency (SFA)
Date Deposited: 30 Jun 2021 00:33
FoR Codes: 30 AGRICULTURAL, VETERINARY AND FOOD SCIENCES > 3005 Fisheries sciences > 300501 Aquaculture @ 100%
SEO Codes: 10 ANIMAL PRODUCTION AND ANIMAL PRIMARY PRODUCTS > 1002 Fisheries - aquaculture > 100202 Aquaculture fin fish (excl. tuna) @ 100%
Downloads: Total: 661
Last 12 Months: 112
More Statistics

Actions (Repository Staff Only)

Item Control Page Item Control Page