Innate resistance of New Zealand paua to abalone viral ganglioneuritis

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Highlights

  • AVG caused by HaHV 1 leads to mortality in all abalone species tested to date.

  • The paua does not present morbidity or mortality after virus challenge.

  • The paua are highly resistant to virus infection and fully resistant to AVG.

Abstract

The susceptibility of New Zealand paua (Haliotis iris) to infection by abalone herpesvirus (Haliotid herpesvirus 1; HaHV) and to the disease abalone viral ganglioneuritis (AVG) was determined. Infection challenges performed by intra-muscular injection and by immersion in infectious water containing HaHV demonstrated that New Zealand paua were highly resistant to infection by Haliotid herpesvirus 1 and were fully resistant to the disease AVG.

Introduction

Global production of farmed abalone has increased significantly over the past 25 years mainly due to high demand from Asian countries. However, the abalone wild-catch sector has experienced a decrease in production due to habitat destruction, overfishing and disease (Cook, 2016). Both wild and farming sectors can be impacted by disease as was observed in Taiwan and Australia during the last decade (Chang et al., 2005, Hooper et al., 2007, Corbeil et al., 2010). In Australia, Haliotid herpesvirus 1 (HaHV) (previously known as abalone herpesvirus; AbHV; family Malacoherpesviridae (Savin et al., 2010)), first observed in land-based farms, spread through wild abalone populations along the coast of the State of Victoria causing the disease known as abalone viral ganglioneuritis (AVG). This resulted in high mortalities and considerable financial losses. During the period 2008–2012 other cases of AVG were reported from processing plants (live holding facilities) and farms in the State of Tasmania, however, extensive surveillance showed that the disease was not present in wild abalone inhabiting Tasmanian waters (Ellard et al., 2012). All Australian abalone species tested to date have been shown to be susceptible to HaHV infection and AVG (Corbeil et al., 2016). In addition, Haliotis diversicolor Reeve 1846 and H. diversicolor supertaxa cultivated in Asia also suffered significant mortalities due to AVG (Wang et al., 2004, Chang et al., 2005). Since its emergence in Australia, research on HaHV has been intense; the viral genome has been sequenced (Savin et al., 2010, Cowley et al., 2012) and many aspects of its biology investigated (Corbeil et al., 2012a, Corbeil et al., 2012b, Crane et al., 2013). The absence of a suitable in vitro system for viral replication has necessitated the development of an in vivo infectivity model to carry out research on, for exemple, viral stability (Corbeil et al., 2012b), host responses (Dang et al., 2013), and determination of susceptibility of abalone species to infection/disease (Corbeil et al., 2012a, Corbeil et al., 2016). Concerns have been raised in relation to an eventual introduction of Haliotid herpesvirus 1 into New Zealand waters where paua (Haliotis iris) constitute an important fishery. The aim of this study was to determine the susceptibility of paua to infection with HaHV and subsequent development of clinical AVG.

Section snippets

Experimental animals

Paua (Haliotis iris) (approximately 50 mm in length) of mixed sex were imported from Moana New Zealand Blue abalone Ltd (Northland, New Zealand). As positive controls to validate the infectivity process, healthy susceptible blacklip (Haliotis rubra) x greenlip (H. laevigata) abalone hybrids (approximately 50 mm in length) were obtained from a local abalone farm (Jade Tiger Pty Ltd, Indented Head, Victoria) which is located in an area of Victoria where there has been no history of AVG. For all

Morbidity/mortality

Following immersion challenge with a 1:2 dilution of HaHV, hybrid abalone showed signs of disease from day 4 post-challenge (22% mortality), reaching a maximum of 78% mortality by day 6. On the other hand, the paua did not show any morbidity/mortality during the period of the trial. There was a statistical difference (p = 0.001) between hybrid and paua mortality curves (Fig. 1). Immersion challenge with the 1:10 dilution of infectious water did not induce mortality in either the hybrids or the

Conclusion

The results presented in this study, including the lack of clinical disease and mortality, as well as low or absent viral load in nerve tissues and reduced prevalence of histological lesions, demonstrate that New Zealand paua (H. iris) are highly resistant to disease, and infection, caused by Haliotid herpesvirus 1 when challenged by immersion and even when injected intra-muscularly. The mechanism underlying the disease resistance remains to be determined, however, further studies at the

Acknowledgments

The authors thank Craig Mostyn Group Jade Tiger abalone Pty Ltd, Indented Head, Victoria, Australia for providing hybrid abalone and Lynette Suvalko and Marama Cribb (Moana New Zealand – Blue Abalone, Northland, New Zealand) for providing the paua. We thank the Ministry of Primary Industries New Zealand (Suzanne Keeling) for facilitating our collaboration with Moana NZ. Lastly, we also thank Jenni Harper and Jean Payne from the AAHL histology laboratory for processing fixed tissue samples. This

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