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Arbovirus Infections As Screening Tools for the Identification of Viral Immunomodulators and Host Antiviral Factors
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Expression dynamics of the aplysia abyssovirus.
Nicholas S Kron1, Benjamin W Neuman2, Sathish Kumar2
1Department of Marine Biology and Ecology, Rosenstiel School of Marine, Atmospheric, and Earth Science, University of Miami, 4600 Rickenbacker Cswy, Miami, FL, USA, 33149.
Virology
|November 11, 2023
Summary
A novel nidovirus, Aplysia abyssovirus 1 (AAbV), is widespread in sea hares, with high RNA levels in healthy animals. Viral replication occurs in gill cells, not neurons, and defective genomes may explain the lack of disease.
Area of Science:
- Marine biology
- Virology
- Invertebrate pathology
Background:
- A novel, extremely large nidovirus, Aplysia abyssovirus 1 (AAbV), was recently identified in RNA sequence databases from Aplysia californica.
- Nidoviruses are known RNA viruses with significant impacts on various hosts.
Purpose of the Study:
- To investigate the distribution and transcriptional dynamics of Aplysia abyssovirus 1 (AAbV) in both maricultured and wild populations of Aplysia californica.
- To understand the cellular localization of viral replication and the nature of viral gene expression.
Main Methods:
- Confirmation of AAbV RNA presence and quantification in sampled animals.
- Transmission electron microscopy (TEM) to identify viral replication sites.
- Analysis of viral transcript splicing patterns.
Main Results:
- AAbV RNA was confirmed to be widespread and present at high levels in apparently healthy Aplysia californica.
- Viral replication factories were identified in ciliated gill epithelial cells, distinct from the primary sites of high viral RNA expression (neurons).
- Viral transcription patterns were consistent with a single leaderless subgenomic RNA, differing from coronaviruses, and suggested high levels of defective genomes in chronically infected individuals.
Conclusions:
- Aplysia abyssovirus 1 (AAbV) is prevalent in Aplysia californica, coexisting with hosts without causing apparent disease.
- The observed viral replication strategy and potential for defective genomes may contribute to the lack of overt pathology despite high viral loads.
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