We have a limited understanding of the specificities of innate immune protection against viral pathogens in non-model invertebrate species, and comparative immunological approaches may offer opportunities to protect agriculturally significant species against viral threats. Haliotid herpesvirus (HaHV-1) is a re-emerging viral pathogen of abalone, with a high mortality rate in wild and farmed species in Australia. This study sought to examine immune priming strategies against this pathogen, and to describe mechanisms of innate immune antiviral protection in this species.
Immune priming with poly(I:C) offered significant protection against HaHV-1 challenge in Australian hybrid abalone a minimum of 72hrs prior to viral challenge. To investigate the antiviral immune gene landscape in this species, the recently available abalone draft genome of the economically important Australian greenlip abalone was subjected to gene mining strategies and domain database analysis, to gain a putative representation of potential key players involved in the greenlip abalone immune response. This was then compared to the better studied mollusc, the oyster. We highlight that these immune counterparts, mainly from the TLR, cytosolic RNA/DNA and RNA interference signalling pathways are highly divergent between the two molluscs, with the oyster closely reflecting that of the mammalian immune response. Interestingly, we identified that STING, a member of the dsDNA sensing pathway is absent in both the greenlip abalone and in a transcriptome assembly of the Australian blacklip abalone, however, is present in the oyster genome, and two additional abalone species (Haliotis rufescens, Haliotis discus hannai). We hypothesise that this may alter susceptibility to HaHV-1 challenge in vivo, however further work needs to be performed to determine this.
This work provides a better understanding of the key features of the abalone antiviral innate immune system, providing key information towards the development of immune priming strategies in these animals.