Journal
JOURNAL OF VIROLOGY
Volume 85, Issue 8, Pages 3959-3967Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.01891-10
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Funding
- USGS Western Fisheries Research Center
- National Institutes of Health R. L. Kirschestein NRSA University of Washington [5 T32 AI007509]
- National Science Foundation [0812603]
- Division Of Environmental Biology
- Direct For Biological Sciences [0812603] Funding Source: National Science Foundation
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The relationship between pathogen fitness and virulence is typically examined by quantifying only one or two pathogen fitness traits. More specifically, it is regularly assumed that within-host replication, as a precursor to transmission, is the driving force behind virulence. In reality, many traits contribute to pathogen fitness, and each trait could drive the evolution of virulence in different ways. Here, we independently quantified four viral infection cycle traits, namely, host entry, within-host replication, within-host coinfection fitness, and shedding, in vivo, in the vertebrate virus Infectious hematopoietic necrosis virus (IHNV). We examined how each of these stages of the viral infection cycle contributes to the fitness of IHNV genotypes that differ in virulence in rainbow trout. This enabled us to determine how infection cycle fitness traits are independently associated with virulence. We found that viral fitness was independently regulated by each of the traits examined, with the largest impact on fitness being provided by within-host replication. Furthermore, the more virulent of the two genotypes of IHNV we used had advantages in all of the traits quantified. Our results are thus congruent with the assumption that virulence and within-host replication are correlated but suggest that infection cycle fitness is complex and that replication is not the only trait associated with virulence.
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