White spot syndrome

White spot syndrome (WSS) is a viral infection of penaeid shrimp. The disease is highly lethal and contagious, killing shrimp quickly. Outbreaks of this disease have wiped out the entire populations of many shrimp farms within a few days, in places throughout the world.

Whispovirus
Virus classification
(unranked): Virus
Realm: incertae sedis
Kingdom: incertae sedis
Phylum: incertae sedis
Class: incertae sedis
Order: incertae sedis
Family: Nimaviridae
Genus: Whispovirus
Species

White spot syndrome virus

White spot syndrome virus (WSSV) is the lone virus (and type species) of the genus Whispovirus (white spot), which is the only genus in the family Nimaviridae.[1] It is responsible for causing white spot syndrome in a wide range of crustacean hosts.[2][3]

The disease is caused by a family of related viruses subsumed as the whitespot syndrome baculovirus complex[4] and the disease caused by them as white spot syndrome.[5]

History

The first reported epidemic due to this virus is from Taiwan in 1992.[6] Reports of losses due to white spot disease came from China in 1993[7] where it led to a virtual collapse of the shrimp farming industry. This was followed by outbreaks in Japan and Korea in the same year, Thailand, India and Malaysia in 1994, and by 1996 it had severely affected East Asia and South Asia. In late 1995, it was reported in the United States, 1998 in Central and South America, 1999 in Mexico, in 2000 in the Philippines, and in 2011 in Saudi Arabia. The virus was detected in Queensland, Australia in November 2016.[8] Australia was believed to be the last shrimp-growing region free from the virus.

Virology

White spot syndrome virus is a species of virus in the genus Whispovirus, in the family Nimaviridae. It is the only species in this family, so serves as the type species.[3][2]

Taxonomy

White spot syndrome virus is a dsDNA virus, which places it in group I of the Baltimore classification system.

Group: dsDNA

[2]

Virion structure

WSSV is a rod-shaped, double-stranded, DNA virus, and the size of the enveloped viral particles have been reported to be 240–380 nm long and 70–159 nm in diameter and nucleocapsid core is 120–205 nm long and 95–165 nm in diameter.[2] The virus has an outer lipid bilayer membrane envelope, sometimes with a tail-like appendage at one end of the virion. The nucleocapsid consists of 15 conspicuous vertical helices located along the long axis; each helix has two parallel striations, composed of 14 globular capsomers, each of which is 8 nm in diameter.[9]

GenusStructureSymmetryCapsidGenomic arrangementGenomic segmentation
WhispovirusOvoidEnvelopedCircularMonopartite

Genome

The complete DNA sequence of the WSSV genome has been assembled into a circular sequence of 292,967 bp.[10] It encodes 531 putative open reading frames.

One of the proteins, WSSV449, has some similarity to host protein Tube and can function like Tube by activating the NF-κB pathway.[11]

Lifecycle

Viral replication is nuclear; DNA-templated transcription is its method. The virus infects an unusually wide host range of crustaceans.[2][3] Transmission of the virus is mainly through oral ingestion and water-borne routes in farms (horizontal transmission) and vertical transmission (from infected mother prawns) in the case of shrimp hatcheries. The virus is present in the wild stocks of shrimp, especially in the coastal waters adjacent to shrimp-farming regions in Asian countries, but mass mortalities of wild shrimp are yet to be observed.

GenusHost detailsTissue tropismEntry detailsRelease detailsReplication siteAssembly siteTransmission
WhispovirusCrustaceansEctoderm; mesodermUnknownUnknownNuclearNuclearContact

Clinical

The virus has a wide host range. While shrimp can survive with the virus for extended periods of time, factors such as stress can cause the outbreak of WSS. The disease is highly virulent and leads to mortality rates of 100% within days in the case of cultured penaeid shrimps. Most of the cultured penaeid shrimps (Penaeus monodon, Marsupenaeus japonicus, Litopenaeus vannamei, and Fenneropenaeus indicus) are natural hosts of the virus. Several nonpenaeid shrimp were also found to be severely infected during experimental challenges. Many crustaceans such as crabs (Scylla spp., Portunus spp.), spiny lobsters (Panulirus spp.), crayfish (Astacus spp.', Cherax spp.) and freshwater shrimp (Macrobrachium spp.) are reported to be infected with variable severities depending on the lifestage of the host and presence of external stressors (temperature, salinity, bacterial diseases, pollutants).

Clinical signs of WSS include a sudden reduction in food consumption, lethargy, loose cuticle and often reddish discolouration, and the presence of white spots of 0.5 to 2.0 mm in diameter on the inside surface of the carapace, appendages, and cuticle over the abdominal segments.[2]

Pathology

In the host, WSSV infects a wide variety of cells from ectodermal and mesodermal origin. Histological changes are seen in the gill epithelium, antennal gland, haematopoeitic tissue, nervous tissue, connective tissue, and intestinal epithelial tissue. Infected cells have prominent intranuclear occlusions that initially stain eosinophilic, but become basophilic with age; hypertrophied nuclei with chromatin margination; and cytoplasmic clearing.[12] Pathogenesis involves widespread tissue necrosis and disintegration.

White spots on the shell of infected shrimp under scanning electron microscope appear as large, dome-shaped spots on the carapace measuring 0.3 to 3.0 mm in diameter. Smaller white spots of 0.02 to 0.10 mm appear as linked spheres on the cuticle surface. Chemical composition of the spots is similar to the carapace, calcium forming 80–90% of the total material, and may have derived from abnormalities of the cuticular epidermis.[13]

Several biochemical changes have been reported after infection with this virus:[14] glucose consumption and plasma lactate concentration increase, glucose 6 phosphate dehydrogenase activity increases, and triglyceride concentration decreases. The voltage-dependent anion channel of the mitochondrion is also upregulated.

Diagnosis

Infection with WSSV differs from other described penaeid infections yellowhead virus (YHV) and infectious hypodermal and hematopoietic necrosis virus (IHHNV) in the described histological findings, as YHV has a reduced tissue specificity, infecting only the intestinal epithelial tissues and IHHNV causes intranuclear occlusions that stain eosinophilic, but do not change over the course of the infection.[12]

Rapid and specific diagnosis of the virus can be accomplished using nested[12] or quantitative PCR.[15]

Treatment

No treatments for WSS are available.

Prevention

A large number of disinfectants are widely used in shrimp farms and hatcheries to prevent an outbreak. Stocking of uninfected shrimp seeds and rearing them away from environmental stressors with extreme care to prevent contamination are useful management measures. Site selection may be one of the most crucial in preventing WSS. Shrimp farmed in areas with relatively low temperature fluctuations and at water temperatures greater than 29°C had increased resistance to WSSV.[16]

References
  1. Wang, HC; Hirono, I; Maningas, MBB; Somboonwiwat, K; Stentiford, G; ICTV Report, Consortium (July 2019). "ICTV Virus Taxonomy Profile: Nimaviridae". The Journal of General Virology. 100 (7): 1053–1054. doi:10.1099/jgv.0.001248. PMID 30924764.
  2. "ICTV Report Nimaviridae".
  3. "Viral Zone". ExPASy. Retrieved 15 June 2015.
  4. "Non-Native Species Summaries: Whitespot Syndrome Baculovirus complex (WSBV)". Gulf States Marine Fisheries Commission. 2003. Archived from the original on October 18, 2005. Retrieved June 30, 2005.
  5. Lightner, D. V. (1996). A handbook of shrimp pathology and diagnostic procedures for diseases of cultured penaeid shrimp. World Aquaculture Society, Baton Rouge, Louisiana, USA.
  6. Chen, S. N. (1995). "Current status of shrimp aquaculture in Taiwan.". In C. L. Browdy; J. S. Hopkins (eds.). Swimming through troubled water. Proceedings of the special session on shrimp farming. Aquaculture ’95. World Aquaculture Society, Baton Rouge, Louisiana, USA. pp. 29–34.
  7. Huang, J.; X. L. Song; J. Yu & C. H. Yang (1995). "Baculoviral hypodermal and hematopoietic necrosis: study on the pathogen and pathology of the explosive epidemic disease of shrimp". Marine Fisheries Research. 16: 1–10.
  8. "White Spot Detected on Queensland Prawn Farm". The Fish Site. December 2, 2016. Retrieved 2016-12-08.
  9. Nadala, E. C. B. Jr.; L. M. Tapay & P. C. Loh (1998). "Characterization of a non-occluded baculovirus-like agent pathogenic to penaeid shrimp". Diseases of Aquatic Organisms. 33 (3): 221–229. doi:10.3354/dao033221. PMID 9745719.
  10. Van Hulten, M. C. W.; J. Witteveldt; S. Peters; N. Kloosterboer; R. Tarchini; F. Fiers; H. Sandbrink; R. K. Lankhorst & J. M. Vlak (2001). "The white spot syndrome virus DNA genome sequence" (PDF). Virology. 286 (1): 7–22. doi:10.1006/viro.2001.1002. PMID 11448154.
  11. Wang, PH; Gu, ZH; Wan, DH; Zhang, MY; Weng, SP; Yu, XQ; He, JG (2011). "The shrimp NF-κB pathway is activated by white spot syndrome virus (WSSV) 449 to facilitate the expression of WSSV069 (ie1), WSSV303 and WSSV371". PLOS ONE. 6 (9): e24773. Bibcode:2011PLoSO...624773W. doi:10.1371/journal.pone.0024773. PMC 3171479. PMID 21931849.
  12. Wongteerasupaya, C.; J. E. Vickers; S. Sriurairatana; G. L. Nash; A. Akarajamorn; V. Boonseang; S. Panyin; A. Tassanakajon; B. Withyachumnarnkul & T. W. Flegel (1995). "A non-occluded, systemic baculovirus that occurs in cells of ectodermal and mesodermal origin and causes high mortality in the black tiger prawn Penaeus monodon". Diseases of Aquatic Organisms. 21: 69–77. doi:10.3354/dao021069.
  13. Wang, C. S.; K. F. Tang; G. H. Kou & S. N. Chen (1997). "Light and electron microscopic evidence of white spot disease in the giant tiger shrimp, Penaeus monodon (Fabricius), and the kuruma shrimp, Penaeus japonicus (Bate), cultured in Taiwan". Journal of Fish Diseases. 20 (5): 323–331. doi:10.1046/j.1365-2761.1997.00301.x.
  14. Chen IT, Aoki T, Huang YT, Hirono I, Chen TC, Huang JY, Chang GD, Lo CF, Wang KC (2011) White spot syndrome virus induces metabolic changes resembling the Warburg effect in shrimp hemocytes in the early stage of infection. J Virol
  15. Dhar, A. K.; M. M. Roux & K. R. Klimpel (2001). "Detection and Quantification of Infectious Hypodermal and Hematopoietic Necrosis Virus and White Spot Virus in Shrimp Using Real-Time Quantitative PCR and SYBR Green Chemistry". Journal of Clinical Microbiology. 39 (8): 2835–2845. doi:10.1128/JCM.39.8.2835-2845.2001. PMC 88247. PMID 11474000.
  16. Kakoolaki, S.; Sharifpour, I.; Afsharnasab, M.; Sepahdari, A.; Mehrabi, M.R.; Ghaednia, B.; Nezamabadi, H. (2014). "Effects of temperature on hematological and histopathological changes and survival rate of juvenile Fenneropenaeus vannamei experimentally challenged to White Spot Virus". Iranian Journal of Fisheries Sciences. 13 (1): 91–102.
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