Abstract
Since its emergence in the 1990s, White Spot Disease (WSD) has had major economic and societal impact in the crustacean aquaculture sector. Over the years shrimp farming alone has experienced billion dollar losses through WSD. The disease is caused by the White Spot Syndrome Virus (WSSV), a large dsDNA virus and the only member of the Nimaviridae family. Susceptibility to WSSV in a wide range of crustacean hosts makes it a major risk factor in the translocation of live animals and in commodity products. Currently there are no effective treatments for this disease. Understanding the molecular basis of disease processes has contributed significantly to the treatment of many human and animal pathogens, and with a similar aim considerable efforts have been directed towards understanding host–pathogen molecular interactions for WSD. Work on the molecular mechanisms of pathogenesis in aquatic crustaceans has been restricted by a lack of sequenced and annotated genomes for host species. Nevertheless, some of the key host–pathogen interactions have been established: between viral envelope proteins and host cell receptors at initiation of infection, involvement of various immune system pathways in response to WSSV, and the roles of various host and virus miRNAs in mitigation or progression of disease. Despite these advances, many fundamental knowledge gaps remain; for example, the roles of the majority of WSSV proteins are still unknown. In this review we assess current knowledge of how WSSV infects and replicates in its host, and critique strategies for WSD treatment.
Highlights
Since its emergence in the early 1990s, White Spot Disease (WSD) has become the greatest threat to global crustacean aquaculture industries [1]
open reading frames (ORF) without polyadenylation signals are usually part of a cluster of ORFs with small intergenic regions and identical transcriptional orientation that can produce polycistronic mRNAs [59,60,61,62]. Translation from these polycistronic mRNAs is likely to be facilitated by internal ribosome entry sites (IRES) [62,63]
A high level of viral protein production can lead to ER stress, e.g., machinery and to make these available White Spot Syndrome Virus (WSSV) can act to halt the cell cycle in activation of unfolded protein response (UPR) pathways
Summary
Since its emergence in the early 1990s, White Spot Disease (WSD) has become the greatest threat to global crustacean aquaculture industries [1]. Viruses 2016, 8, 23 are susceptible to WSSV infection and disease Natural populations of these hosts can act as reservoirs for this pathogen [11,12]. Economic drivers have focused research on WSD in farmed shrimp; the host range of WSSV includes many other decapod and non-decapod species including crabs, lobsters, prawns, crayfishes, and copepods [18,25]. This is fundamental for advancing our understanding of and the host innate immune system (Li et al [45], Shekhar and Ponniah [46], Sanchez-Paz [47], and Sritunyalucksana et al [48]) but the interactions between WSSV and the host intracellular environment have received less attention This is fundamental for advancing our understanding of the WSD infection process and exploring potential opportunities for disease treatment and prevention. We investigate the current treatment options that have been explored and consider possible future directions for advancing disease treatment and mitigation
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
