Data from: Trade-offs and mixed infections in an obligate-killing insect pathogen

Natural populations of pathogens are frequently composed of numerous
interacting strains. Understanding what maintains this diversity remains a
key focus of research in disease ecology. In addition, within-host
pathogen dynamics can have a strong impact on both infection outcome and
the evolution of pathogen virulence and thus understanding the impact of
pathogen diversity is important for disease management. We compared eight
genetically distinguishable variants from Spodoptera exempta
nucleopolyhedrovirus (SpexNPV) isolated from the African armyworm,
Spodoptera exempta. NPVs are obligate killers and the vast majority of
transmission-stages are not released until after the host has died. The
NPV variants differed significantly in their virulence and could be
clustered into two groups based on their dose-response curves. They also
differed in their speed of kill and productivity (transmission potential)
for S. exempta. The mixed-genotype wild-type SpexNPV, from which each
variant was isolated, was significantly more virulent than any individual
variant and its mean mortality rate was within the fastest group of
individual variants. However, the wild-type virus produced fewer new
infectious stages than any single variant, which might reflect competition
among the variants. A survival analysis, combining the mortality and speed
of kill data, confirmed the superiority of the genetically-mixed wild-type
virus over any single variant. S. exempta larvae infected with wild-type
SpexNPV were predicted to die 2.7 and 1.9 times faster than insects
infected with isolates from either of the two clusters of genotypes.
Theory suggests that there are likely to be trade-offs between pathogen
fitness traits. Across all larvae, there was a negative linear
relationship between virus yield and speed of kill, such that more rapid
host death carried the cost of producing fewer transmission stages. We
also found a near-significant relationship for the same trend at the
inter-variant level. However, there was no evidence for a significant
relationship between the induced level of mortality and transmission
potential (virus yield) or speed of kill.