Prevalence of nervous necrosis virus (NNV) and Streptococcus species in wild marine fish and crustaceans from the Levantine Basin, Mediterranean Sea

Betanodaviruses, the causal agents of viral nervous necrosis in marine fish, have bipartite, positive-sense RNA genomes. As their genomes are the smallest and simplest among viruses, betanodaviruses have been studied in detail as model viruses by using a genetic-engineering system, as has occurred with the insect alphanodaviruses, the other members of the family Nodaviridae. However, studies of virus–host interactions have been limited, as betanodaviruses basically infect marine fish at early developmental stages (larval and juvenile). These fish are only available for a few months of the year and are not suitable for the construction of a reverse-genetics system. To overcome these problems, several freshwater fish species were tested for their susceptibility to betanodaviruses. It was found that adult medaka (Oryzias latipes), a well-known model fish, was susceptible to both Striped jack nervous necrosis virus (the type species of the genus Betanodavirus) and Redspotted grouper nervous necrosis virus (RGNNV), which have different host specificities in marine fish species. Infected medaka exhibited erratic swimming and the viruses were localized specifically in the brain, spinal cord and retina of the infected fish, similar to the pattern of infection in naturally infected marine fish. Moreover, medaka were susceptible to RGNNV at the larval stage. This is the first report of a model virus–model host infection system in fish. This system should facilitate elucidation of the mechanisms underlying RNA virus infections in fish.

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Nervous Necrosis Virus Coat Protein Mediates Host Translation Shutoff through Nuclear Translocalization and Degradation of Polyadenylate Binding Protein

Journal of Virology ◽

10.1128/jvi.02364-20 ◽

2021 ◽

Author(s):

Chao-An Cheng ◽

Jia-Ming Luo ◽

Ming-Hsien Chiang ◽

Kuei-Yuan Fang ◽

Chen-Hung Li ◽

...

Keyword(s):

Coat Protein ◽

Marine Fish ◽

Molecular Mechanisms ◽

Fish Larvae ◽

Binding Protein ◽

Economic Damage ◽

Brain Cells ◽

Nervous Necrosis Virus ◽

Epinephelus Coioides ◽

Necrosis Virus

Nervous necrosis virus (NNV) belongs to the Betanodavirus genus of the Nodaviridae family and is the main cause of viral nervous necrosis disease in marine fish larvae and juveniles worldwide. The NNV virion contains two positive-sense, single-stranded RNA genomes, which encode RNA-dependent RNA polymerase, coat protein and B2 protein. Interestingly, NNV infection can shut off host translation in orange-spotted grouper ( Epinephelus coioides ) brain cells, however, the detailed mechanisms of this action remain unknown. In this study, we discovered that the host translation factor, polyadenylate binding protein (PABP), is a key target during NNV takeover of host translation machinery. Additionally, ectopic expression of NNV coat protein is sufficient to trigger nuclear translocalization and degradation of PABP, followed by translation shutoff. A direct interaction between NNV coat protein and PABP was demonstrated, and this binding requires the NNV coat protein N-terminal shell domain and PABP proline-rich linker region. Notably, we also showed that degradation of PABP during later stages of infection is mediated by the ubiquitin-proteasome pathway. Thus, our study reveals that the NNV coat protein hijacks host PABP, causing its relocalization to the nucleus and promoting its degradation to stimulate host translation shutoff. IMPORTANCE Globally, more than 200 species of aquacultured and wild marine fish are susceptible to NNV infection. Devastating outbreaks of this virus have been responsible for massive economic damage in the aquaculture industry, but the molecular mechanisms by which NNV affects its host remain largely unclear. In this study, we show that NNV hijacks translation in host brain cells, with the viral coat protein binding to host PABP to promote its nuclear translocalization and degradation. This previously unknown mechanism of NNV-induced host translation shutoff greatly enhances the understanding of NNV pathogenesis and provides useful insights and novel tools for development of NNV treatments, such as the use of orange-spotted grouper brain cells as an in vitro model system.

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Indigenous versus Lessepsian Hosts: Nervous Necrosis Virus (NNV) in Eastern Mediterranean Sea Fish

Viruses ◽

10.3390/v12040430 ◽

2020 ◽

Vol 12 (4) ◽

pp. 430 ◽

Cited By ~ 1

Author(s):

Yael Lampert ◽

Ran Berzak ◽

Nadav Davidovich ◽

Arik Diamant ◽

Nir Stern ◽

...

Keyword(s):

Invasive Species ◽

Mediterranean Sea ◽

Marine Environment ◽

Fish Species ◽

Eastern Mediterranean ◽

Nervous Necrosis Virus ◽

Indigenous Species ◽

Necrosis Virus ◽

Marine Aquaculture ◽

The Mediterranean

Viruses are among the most abundant and diverse biological components in the marine environment. In finfish, viruses are key drivers of host diversity and population dynamics, and therefore, their effect on the marine environment is far-reaching. Viral encephalopathy and retinopathy (VER) is a disease caused by the marine nervous necrosis virus (NNV), which is recognized as one of the main infectious threats for marine aquaculture worldwide. For over 140 years, the Suez Canal has acted as a conduit for the invasion of Red Sea marine species into the Mediterranean Sea. In 2016–2017, we evaluated the prevalence of NNV in two indigenous Mediterranean species, the round sardinella (Sardinella aurita) and the white steenbras (Lithognathus mormyrus) versus two Lessepsian species, the Randall’s threadfin bream (Nemipterus randalli) and the Lessepsian lizardfish (Saurida lessepsianus). A molecular method was used to detect NNV in all four fish species tested. In N. randalli, a relatively newly established invasive species in the Mediterranean Sea, the prevalence was significantly higher than in both indigenous species. In S. lessepsianus, prevalence varied considerably between years. While the factors that influence the effective establishment of invasive species are poorly understood, we suggest that the susceptibility of a given invasive fish species to locally acquired viral pathogens such as NVV may be important, in terms of both its successful establishment in its newly adopted environment and its role as a reservoir ‘host’ in the new area.

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