Abstract
The context-dependent investigations of host–pathogen genotypic interactions, where environmental factors are explicitly incorporated, allow the assessment of both coevolutionary history and contemporary ecological influences. Such a functional explanatory framework is particularly valuable for describing mortality trends and identifying drivers of disease risk more accurately. Using two common North American frog species (Lithobates pipiens and Lithobates sylvaticus) and three strains of frog virus 3 (FV3) at different temperatures, we conducted a laboratory experiment to investigate the influence of host species/genotype, ranavirus strains, temperature, and their interactions, in determining mortality and infection patterns. Our results revealed variability in host susceptibility and strain infectivity along with significant host–strain interactions, indicating that the outcome of an infection is dependent on the specific combination of host and virus genotypes. Moreover, we observed a strong influence of temperature on infection and mortality probabilities, revealing the potential for genotype–genotype–environment interactions to be responsible for unexpected mortality in this system. Our study thus suggests that amphibian hosts and ranavirus strains genetic characteristics should be considered in order to understand infection outcomes and that the investigation of coevolutionary mechanisms within a context-dependent framework provides a tool for the comprehensive understanding of disease dynamics.
Highlights
Despite a century of relatively efficient control and prevention, the last three decades have witnessed the increasing emergence and re-emergence of infectious diseases (Cohen 2000)
Three different frog virus 3 (FV3)-like viruses were chosen for this study: (i) the original FV3 isolate that was first isolated in 1965 (Granoff et al 1965) is known to infect both Lithobates pipiens and L. sylvaticus (Duffus et al 2008). (ii) a more recent variant that is defective in its ability to methylate the viral genome and may trigger a TLR-9 response, might be the least virulent, and (iii) an FV3-like isolate designated Spotted salamander Maine Virus (SsMeV, US National Wildlife Health Center #1591903 + 08) which was isolated during an outbreak involving frogs and salamanders from Connor Township, Aroostook County, Maine in July 1998
Nucleotide sequence analysis of the major capside protein gene (MCP) suggests that SsMeV is an FV3-like virus and recent 454 GS-FLX sequencing suggests that SsMeV is 98.79% identical to FV3 at the nucleotide level but differ in several Open Reading Frame (ORF) coding regions possibly involved in infectivity (Morrison et al 2014)
Summary
Despite a century of relatively efficient control and prevention, the last three decades have witnessed the increasing emergence and re-emergence of infectious diseases (Cohen 2000). Emerging infectious diseases (EIDs) are caused by pathogens that have recently increased in incidence, expanded their host or geographic range, have been newly discovered, or are caused by a newly evolved agent (Daszak et al 2000). The emergence of viruses, such as Nipah, Hendra, SARS, and avian influenza A to name a few, has increased scientific and public awareness regarding the threats of infectious diseases and their possible detrimental consequences for biodiversity, ecosystem functioning, and public health (Daszak et al 2000; Binder et al 1999; Morens et al 2004). The increasing occurrence of pathogens crossing the barriers between their natural reservoirs to human populations (zoonosis), has boosted research on wildlife diseases (Antia et al 2003). Diseases contribute to species extinctions (MacPhee and Greenwood 2013) especially in cases where
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