Interleukin-1β secreted from betanodavirus-infected microglia caused the death of neurons in giant grouper brains

Chiang, Yu-Hui; Wu, Yuchi; Chi, Shau-Chi

doi:10.1016/j.dci.2017.01.002

Cited by 24 publications

(12 citation statements)

References 43 publications

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“…This result was corroborated in an experimental infection performed on sea bass with an RGNNV recombinant strain harboring the same mutations in the capsid protein [221] because low or no inflammatory induction (transcription of mxA, isg 15 and tnf alpha genes) was observed in the brain of fish infected with the mutant strain, whereas a strong induction was observed in fish challenged with the wt isolate. Finally, a similar result was observed in primary cultures of grouper brain cells, where NNV infection may activate microglial proliferation and stimulate microglial secretion of interleukin (IL)-1b, which is a critical cytokine responsible for neuronal death [242].…”

Section: Host Responsesupporting

confidence: 65%

Betanodavirus and VER Disease: A 30-year Research Review

2020

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The outbreaks of viral encephalopathy and retinopathy (VER), caused by nervous necrosis virus (NNV), represent one of the main infectious threats for marine aquaculture worldwide. Since the first description of the disease at the end of the 1980s, a considerable amount of research has gone into understanding the mechanisms involved in fish infection, developing reliable diagnostic methods, and control measures, and several comprehensive reviews have been published to date. This review focuses on host-virus interaction and epidemiological aspects, comprising viral distribution and transmission as well as the continuously increasing host range (177 susceptible marine species and epizootic outbreaks reported in 62 of them), with special emphasis on genotypes and the effect of global warming on NNV infection, but also including the latest findings in the NNV life cycle and virulence as well as diagnostic methods and VER disease control.

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Section: Host Responsesupporting

confidence: 65%

Betanodavirus and VER Disease: A 30-year Research Review

2020

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“…Conversely, the early larval hindbrain injection with bacteria mobilized peripheral macrophages into the infection site ( 50 ). Chiang and coworkers demonstrated that NNV infection of the primary culture of brain cells from giant grouper ( Epinephelus lanceolatus ) activates microglial cell proliferation and secretion of proinflammatory cytokines (IL-1β and TNF-α) and subsequently the neural cell death ( 51 ). Involvement of microglia in neuroinflammation in fish upon bacterial infection with Weissella cibaria has also been described in vitro using microglia cultures isolated from the brain of Nile tilapia ( 52 ).…”

Section: Discussionmentioning

confidence: 99%

Tilapia Lake Virus-Induced Neuroinflammation in Zebrafish: Microglia Activation and Sickness Behavior

et al. 2021

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In mammals, the relationship between the immune system and behavior is widely studied. In fish, however, the knowledge concerning the brain immune response and behavioral changes during brain viral infection is very limited. To further investigate this subject, we used the model of tilapia lake virus (TiLV) infection of zebrafish (Danio rerio), which was previously developed in our laboratory. We demonstrated that TiLV persists in the brain of adult zebrafish for at least 90 days, even when the virus is not detectable in other peripheral organs. The virions were found in the whole brain. During TiLV infection, zebrafish displayed a clear sickness behavior: decreased locomotor activity, reduced food intake, and primarily localizes near the bottom zone of aquaria. Moreover, during swimming, individual fish exhibited also unusual spiral movement patterns. Gene expression study revealed that TiLV induces in the brain of adult fish strong antiviral and inflammatory response and upregulates expression of genes encoding microglia/macrophage markers. Finally, using zebrafish larvae, we showed that TiLV infection induces histopathological abnormalities in the brain and causes activation of the microglia which is manifested by changes in cell shape from a resting ramified state in mock-infected to a highly ameboid active state in TiLV-infected larvae. This is the first study presenting a comprehensive analysis of the brain immune response associated with microglia activation and subsequent sickness behavior during systemic viral infection in zebrafish.

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“…NNV causes neurons destruction by infection, and the virus replication results in vacuolation of the fish brain. In addition, it has been suggested that the observed damage could be the result of the brain inflammatory response since inflammation constitutes a defense mechanism against pathogens, but it may also damage cells and tissues [61]. Brain and eyes have been characterized as immune-privileged organs [62].…”

Section: Discussionmentioning

confidence: 99%

Transcriptomic Analysis of Fish Hosts Responses to Nervous Necrosis Virus

2022

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Nervous necrosis virus (NNV) has been responsible for mass mortalities in the aquaculture industry worldwide, with great economic and environmental impact. The present review aims to summarize the current knowledge of gene expression responses to nervous necrosis virus infection in different fish species based on transcriptomic analysis data. Four electronic databases, including PubMed, Web of Science, and SCOPUS were searched, and more than 500 publications on the subject were identified. Following the application of the appropriate testing, a total of 24 articles proved eligible for this review. NNV infection of different host species, in different developmental stages and tissues, presented in the eligible publications, are described in detail, revealing and highlighting genes and pathways that are most affected by the viral infection. Those transcriptome studies of NNV infected fish are oriented in elucidating the roles of genes/biomarkers for functions of special interest, depending on each study’s specific emphasis. This review presents a first attempt to provide an overview of universal host reaction mechanisms to viral infections, which will provide us with new perspectives to overcome NNV infection to build healthier and sustainable aquaculture systems.

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Interleukin-1β secreted from betanodavirus-infected microglia caused the death of neurons in giant grouper brains

Cited by 24 publications

References 43 publications

Betanodavirus and VER Disease: A 30-year Research Review

Betanodavirus and VER Disease: A 30-year Research Review

Tilapia Lake Virus-Induced Neuroinflammation in Zebrafish: Microglia Activation and Sickness Behavior

Transcriptomic Analysis of Fish Hosts Responses to Nervous Necrosis Virus

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