About
Ranaviruses
Large, double-stranded DNA viruses in the genus Ranavirus (Family Iridoviridae) that infect amphibians, reptiles and fish.
What are ranaviruses?
Ranaviruses are large, double-stranded viruses in the genus Ranavirus (Family Iridoviridae) that infect amphibians, reptiles and fish. Remarkably, some ranaviruses can be transmitted among these three vertebrate classes.
They have been associated with die-offs in larval and adult amphibians in the Americas, Europe, and Asia, and in wild and cultured fish populations worldwide. While ranaviruses have been reported from reptiles in captivity for years, there are a growing number of reports of morbidity and mortality in free-ranging populations as well.
Ranaviruses are also moved regionally and internationally in animal trade. Ranaviruses are a substantial and growing risk to aquaculture and global biodiversity.
Ranavirus Book
Distribution & Conservation
Ranaviruses have a truly global distribution. For instance, ranaviruses are known to infect at least 91 amphibian species in 14 families from North and South America, Europe, Asia, Australia, and, recently, Africa. Similarly ranaviruses have been identified in aquaculture and in wild fishes in North America, Europe, Asia, and Australia. Several studies have found ranavirus-infected animals in the international commercial trade of amphibians, reptiles, and fishes. Overall, ranavirus has been found in at least 173 ectothermic vertebrates from at least 32 nations around the world.
Ranaviruses are a ‘Notifiable Pathogen’ by the OIE (the World Organization for Animal Health) and must be reported to the OIE by member countries.
Populations of the European common frog, Rana temporaria, have declined with the emergence of ranaviruses in England. (Photo: Richard Bartz, Wikimedia commons)
Because of their broad distribution, large host range, and often high virulence, ranaviruses have the potential to be important threats to some amphibians, fishes, and reptiles. In the United Kingdom, for instance, a ranavirus has been associated with widespread declines of the common frog, Rana temporaria, and frequent die-offs in other amphibians may be associated with local extirpation. Ranavirus-associated die-offs have been observed in populations of Eastern Box Turtles (Terrapene carolina carolina) in several areas in the eastern United states. Turtles often require many years to reach sexual maturity and have little recruitment in any given year. These life history traits are offset by normally very high adult survival. Turtles may be poorly equipped to buffer large ranavirus epidemics in adults like those seen in recent years.
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For more information see:
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Gray, M. J., D. L. Miller, and J. T. Hoverman. 2009. Ecology and pathology of amphibian ranaviruses. Diseases of Aquatic Organisms 87:243-266.
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Miller, D., M. Gray, and A. Storfer. 2011. Ecopathology of ranaviruses infecting amphibians. Viruses 3:2351-2373.
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Schloegel, L. M., P. Daszak, A. A. Cunningham, R. Speare, and B. Hill. 2010. Two amphibian diseases, chytridiomycosis and ranaviral disease, are now globally notifiable to the world organization for animal health (OIE): An assessment. Diseases of Aquatic Organisms 92:101-108.
Ecology & Evolution
Ranaviruses are transmitted by direct contact, through the water, and by consuming infected tissues or fomites. The duration and outcome of ranavirus infection varies among host species, developmental stage, and temperature and probably many other environmental factors. In amphibians, most mortality events have been associated with larvae (tadpoles) at breeding sites, with larvae generally being more susceptible than adults. It is not known whether this pattern holds in fish and reptiles.
Several studies have found that amphibians exposed to anthropogenic “stressors,” such as herbicides and insecticides or even cattle access to a pond can make individuals more susceptible to ranaviruses or epidemics more severe. However natural “stressors,” such as the presence of aquatic predators, do not appear to have similar effects on susceptibility. Importantly, ranaviruses are not universally lethal, even in highly susceptible species and stages. Low-level, sublethal infections appear to be common in at least some taxa. This may help explain how ranaviruses persist between outbreaks, although persistence outside the host in the environment has not been entirely ruled out. The evolutionary history of ranaviruses is currently being worked out, but it seems that there have been at least a couple of “jumps” from one host taxa to another (e.g., fish to frogs). There is also evidence of local coevolution between tiger salamanders in western North America and their viruses.
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For more information see:
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Gahl, M. K., and A. J. K. Calhoun. 2010. The role of multiple stressors in ranavirus-caused amphibian mortalities in Acadia national park wetlands. Canadian Journal of Zoology 88:108-121.
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Gray, M. J., D. L. Miller, and J. T. Hoverman. 2009. Ecology and pathology of amphibian ranaviruses. Diseases of Aquatic Organisms 87:243-266.
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Hoverman, J. T., M. J. Gray, N. A. Haislip, and D. L. Miller. 2011. Phylogeny, life history, and ecology contribute to differences in amphibian susceptibility to ranaviruses. EcoHealth 8:301-319.
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Jancovich, J. K., M. Bremont, J. W. Touchman, and B. L. Jacobs. 2010. Evidence for multiple recent host species shifts among the ranaviruses (family Iridoviridae). Journal of Virology 84:2636-2647.
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Miller, D., M. Gray, and A. Storfer. 2011. Ecopathology of ranaviruses infecting amphibians. Viruses 3:2351-2373.
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Reeve, B. C., E. J. Crespi, C. M. Whipps, and J. L. Brunner. 2013. Natural stressors and ranavirus susceptibility in larval wood frogs (_Rana sylvatica_). EcoHealth 10:190-200.
Virology & Immunology
Ranaviruses are large, double-stranded DNA viruses. Their ~150 nm, icosahedral capsid can be seen in the cytoplasm of infected cells with electron microscopy, often in paracrystaline arrays. Their ~105 kbp genome, which encodes ~100 genes, comprises a single linear, but circularly permuted, element. The unique replication cycle of ranaviruses (and the other vertebrate iridoviruses) involves both nuclear and cellular phases, which results in a plasmalipid envelope, which is derived from the nuclear membrane, internal to the protein capsid. The capsid may be enveloped, if it buds from the host cell membrane, or naked if the host cell lyses.
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For more information see:
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Chen, G., and J. Robert. 2011. Antiviral immunity in amphibians. Viruses 3:2065-2086.
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Chinchar VG (2002) Ranaviruses (family Iridoviridae): Emerging cold-blooded killers. Archives of Virology 147:447–470.
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Whittington, R. J., J. A. Becker, and M. M. Dennis. 2010. Iridovirus infections in finfish — critical review with emphasis on ranaviruses. Journal of Fish Diseases 33:95-122.
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Williams, T., V. Barbosa-Solomieu, and V. G. Chinchar. 2005. A decade of advances in iridovirus research. Advances in Virus Research 65:173-248.