Distribution and Host Range of Ranaviruses

Duffus, Amanda L. J.; Waltzek, Thomas B.; Stöhr, Anke C.; Allender, Matthew C.; Gotesman, Michael; Whittington, Richard J.; Hick, Paul; Hines, Megan K.; Marschang, Rachel E.

doi:10.1007/978-3-319-13755-1_2

Cited by 136 publications

(185 citation statements)

References 180 publications

(256 reference statements)

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“…Ranaviruses are emerging pathogens that infect amphibians, fish, and reptiles (Duffus et al 2015). Frog virus 3 (FV3) is the type species for the genus Ranavirus (Jancovich et al 2015) and has been shown to replicate faster in host cells in vitro with increasing temperature (Ariel et al 2009).…”

Section: Introduction and Purposementioning

confidence: 99%

Water Temperature Affects Susceptibility to Ranavirus

et al. 2016

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The occurrence of emerging infectious diseases in wildlife populations is increasing, and changes in environmental conditions have been hypothesized as a potential driver. For example, warmer ambient temperatures might favor pathogens by providing more ideal conditions for propagation or by stressing hosts. Our objective was to determine if water temperature played a role in the pathogenicity of an emerging pathogen (ranavirus) that infects ectothermic vertebrate species. We exposed larvae of four amphibian species to a Frog Virus 3 (FV3)-like ranavirus at two temperatures (10 and 25°C). We found that FV3 copies in tissues and mortality due to ranaviral disease were greater at 25°C than at 10°C for all species. In a second experiment with wood frogs (Lithobates sylvaticus), we found that a 2°C change (10 vs. 12°C) affected ranaviral disease outcomes, with greater infection and mortality at 12°C. There was evidence that 10°C stressed Cope's gray tree frog (Hyla chrysoscelis) larvae, which is a species that breeds during summer-all individuals died at this temperature, but only 10% tested positive for FV3 infection. The greater pathogenicity of FV3 at 25°C might be related to faster viral replication, which in vitro studies have reported previously. Colder temperatures also may decrease systemic infection by reducing blood circulation and the proportion of phagocytes, which are known to disseminate FV3 through the body. Collectively, our results indicate that water temperature during larval development may play a role in the emergence of ranaviruses.

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Section: Introduction and Purposementioning

confidence: 99%

Water Temperature Affects Susceptibility to Ranavirus

et al. 2016

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“…Over the last 50 years, infections caused by ranaviruses ( Iridoviridae ) in most part of the world have markedly increased in prevalence as well as in the range of species infected (Chinchar et al, 2009; Duffus et al, 2015; Kik et al, 2011; Kolby et al, 2014; Kolby et al, 2015; Price et al, 2014). Emerging infectious diseases caused by ranavirus are not only alarming for biodiversity and aquaculture, but also poses fundamental issues related to the evolution of host/pathogen interactions (Chen and Robert, 2012; Collins; Daszak et al, 1999; Gray et al, 2009; Robert and Gregory Chinchar, 2012).…”

Section: Introductionmentioning

confidence: 99%

Xenopus-FV3 host-pathogen interactions and immune evasion

et al. 2017

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We first review fundamental insights into anti-ranavirus immunity learned with the Xenopus laevis/ranavirus FV3 model that are generally applicable to ectothermic vertebrates. We then further investigate FV3 genes involved in immune evasion. Focusing on FV3 knockout (KO) mutants defective for a putative viral caspase activation and recruitment domain-containing (CARD)-like protein (Δ64R-FV3), a β-hydroxysteroid dehydrogenase homolog (Δ52L-FV3), and an immediate-early 18kDa protein (FV3-Δ18K), we assessed the involvement of these viral genes in replication, dissemination and interaction with peritoneal macrophages in tadpole and adult frogs. Our results substantiate the role of 64R and 52L as critical immune evasion genes, promoting persistence and dissemination in the host by counteracting type III IFN in tadpoles and type I IFN in adult frogs. Comparably, the substantial accumulation of genome copy numbers and exacerbation of type I and III IFN gene expression responses but deficient release of infectious virus suggests that 18K is a viral regulatory gene.

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“…Ranaviruses such as Frog Virus 3 (FV3) are emerging pathogens that cause severe morbidity and mortality among fish, amphibians and reptiles worldwide (Chinchar et al, 2009; Duffus et al, 2015). The increase in prevalence and the expansion of host range suggests that ranaviruses are successful in overcoming host immune defenses.…”

Section: Introductionmentioning

confidence: 99%

Characterization of Frog Virus 3 knockout mutants lacking putative virulence genes

et al. 2015

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To identify ranavirus virulence genes, we engineered Frog Virus 3 (FV3) knockout (KO) mutants defective for a putative viral caspase activation and recruitment domain-containing (CARD) protein (Δ64R-FV3) and a β-hydroxysteroid dehydrogenase homolog (Δ52L-FV3). Compared to wild type (WT) FV3, infection of Xenopus tadpoles with Δ64R- or Δ52L-FV3 resulted in significantly lower levels of mortality and viral replication. We further characterized these and two earlier KO mutants lacking the immediate-early18 kDa protein (FV3-Δ18K) or the truncated viral homolog of eIF-2α (FV3-ΔvIF-2α). All KO mutants replicated as well as WT-FV3 in non-amphibian cell lines, whereas in Xenopus A6 kidney cells replication of ΔvCARD-, ΔvβHSD- and ΔvIF-2α-FV3 was markedly reduced. Furthermore, Δ64R- and ΔvIF-2α–FV3 were more sensitive to interferon than WT and Δ18-FV3. Notably, Δ64R-, Δ18K- and ΔvIF-2α- but not the Δ52L-FV3 triggered more apoptosis than WT FV3. These data suggest that vCARD (64R) and vβ-HSD (52L) genes contribute to viral pathogenesis.

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Distribution and Host Range of Ranaviruses

Cited by 136 publications

References 180 publications

Water Temperature Affects Susceptibility to Ranavirus

Water Temperature Affects Susceptibility to Ranavirus

Xenopus-FV3 host-pathogen interactions and immune evasion

Characterization of Frog Virus 3 knockout mutants lacking putative virulence genes

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