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Review
. 2020 Feb 9;9(2):106.
doi: 10.3390/pathogens9020106.

Betanodavirus and VER Disease: A 30-year Research Review

Isabel Bandín  1 , Sandra Souto  1
Affiliations
Review

Betanodavirus and VER Disease: A 30-year Research Review

Isabel Bandín et al. Pathogens. .

Abstract

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.

Keywords: control; diagnostics; epizootiology; nervous necrosis virus (NNV); viral encephalopathy and retinopathy (VER); virus–host interaction.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
Schematic overview of the betanodavirus replication cycle: After entry, the viral bisegmented single stranded (+) RNA genome is released into the cytoplasm. Subsequently, host ribosomes translate the viral RNA1 into the viral RNA-dependent RNA polymerase (RdRp) (A). The RdRp is then used to copy the genomic (+) RNA1, synthetizing a (−) RNA strand and generating a dsRNA (B). The dsRNA is now used for replication/transcription into new RNA1 molecules (C), all this process takes place in association with outer mitochondrial membranes. Afterwards, a sub-genomic RNA, namely RNA3, is synthesized from the 3’ terminus of RNA1(D). RNA3 encodes -and is translated into- the two small proteins B1 and B2 (E) which show nuclear localization. In addition, RNA3, presumably like in alfanodavirus, also regulates RNA2 synthesis (F) and it is downregulated at the onset of RNA2 replication/transcription (dotted line). RNA2 translation yields the capsid protein (G) and, finally, nascent (+) RNA1 and (+) RNA2 molecules are packaged into progeny virions (H). Adapted from SMART (Servier Medical Art), licensed under a Creative Common Attribution 3.0 Generic License. http://smart.servier.com/.
Figure 2
Figure 2
Distribution of Nervous necrosis virus (NNV) genotypes. Adapted from SMART (Servier Medical Art), licensed under a Creative Common Attribution 3.0 Generic License. http://smart.servier.com/.
See this image and copyright information in PMC

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