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. 2017 Jul 26;284(1859):20171090.
doi: 10.1098/rspb.2017.1090.

Stress hormones predict a host superspreader phenotype in the West Nile virus system

Stephanie S Gervasi  1 , Sarah C Burgan  2 , Erik Hofmeister  3 , Thomas R Unnasch  4 , Lynn B Martin  5
Affiliations

Stress hormones predict a host superspreader phenotype in the West Nile virus system

Stephanie S Gervasi et al. Proc Biol Sci. .

Abstract

Glucocorticoid stress hormones, such as corticosterone (CORT), have profound effects on the behaviour and physiology of organisms, and thus have the potential to alter host competence and the contributions of individuals to population- and community-level pathogen dynamics. For example, CORT could alter the rate of contacts among hosts, pathogens and vectors through its widespread effects on host metabolism and activity levels. CORT could also affect the intensity and duration of pathogen shedding and risk of host mortality during infection. We experimentally manipulated songbird CORT, asking how CORT affected behavioural and physiological responses to a standardized West Nile virus (WNV) challenge. Although all birds became infected after exposure to the virus, only birds with elevated CORT had viral loads at or above the infectious threshold. Moreover, though the rate of mortality was faster in birds with elevated CORT compared with controls, most hosts with elevated CORT survived past the day of peak infectiousness. CORT concentrations just prior to inoculation with WNV and anti-inflammatory cytokine concentrations following viral exposure were predictive of individual duration of infectiousness and the ability to maintain physical performance during infection (i.e. tolerance), revealing putative biomarkers of competence. Collectively, our results suggest that glucocorticoid stress hormones could directly and indirectly mediate the spread of pathogens.

Keywords: competence; glucocorticoid; resistance; tolerance; transmission.

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Conflict of interest statement

We declare we have no competing interests.

Figures

Figure 1.
Figure 1.
Effects of experimental corticosterone (CORT) treatment on zebra finch survival after exposure to West Nile virus (WNV). CORT treatment predicted survival rate of zebra finch hosts exposed to WNV (formula image, p = 0.029). The grey shaded bar between 4 and 6 days-post-inoculation on the x-axis indicates the period of peak infection intensity detected via quantitative-PCR in CORT+ and CORT++ hosts. The black, large-dashed line at the top (no mortality) corresponds to the control treatment; the blue, large-dashed line (middle) corresponds to the CORT+ treatment, and the red dotted line corresponds to the CORT++ treatment. (Online version in colour.)
Figure 2.
Figure 2.
Viremia of zebra finches exposed to WNV across different experimental CORT treatments. CORT treatment (formula image, p < 0.0001), time (formula image, p < 0.0001) and the interaction between treatment and time (formula image, p < 0.0001) predicted host viremia. At peak viremia levels, hosts in the CORT+ and CORT++ treatments (square and triangle symbols, respectively) had viral infection intensities that were approximately 2 orders of magnitude greater than those of control birds (circle symbols). The horizontal dashed line at 105 pfu WNV ml−1 indicates the proposed threshold for transmission of WNV from bird to mosquito; only birds in the elevated CORT treatments attained viremia levels above this transmission threshold. Points represent averages at sampled time points over the study. Error bars are ±1 s.e. of the mean. (Online version in colour.)
Figure 3.
Figure 3.
Pre-inoculation CORT concentrations (after hormone manipulation and just before WNV inoculation) positively predicted host infectiousness (i.e. the number of days a host was detected with viremia levels at or above the 105 pfu ml−1 transmission threshold). Higher pre-inoculation CORT concentrations were associated with longer infectiousness (p = 0.01 for main effect of CORT concentration by comparing alternative zero-inflated generalized linear models with a Poisson distribution with and without this explanatory factor; β = 14.59 ± 7.45, p = 0.050 for null hypothesis of slope = 0 for CORT effect on days infectious). The effects display is based on the full model predicting infectiousness (which included CORT concentration, IFN-γ expression, IL-10 expression, and the interactions between CORT and each cytokine; see text and electronic supplementary material, table S2). The line depicts the estimates (based on a GLM with a Poisson distribution, no zero inflation) and the shaded region represents the 95% confidence interval around the estimated effect of CORT concentration on days infectious. The vertical axis is labelled on the response variable scale and effects are plotted on the scale of the linear predictor (i.e. effects are plotted on the log scale).
Figure 4.
Figure 4.
Individual pre-inoculation CORT concentration negatively predicted the ability to maintain vertical flight during WNV infection (F1,12 = 11.01, p = 0.006); higher pre-inoculation CORT concentrations were associated with reduced individual flight tolerance. In the effects display, the line depicts estimates and the shaded area represents the 95% confidence interval around the estimated effect of the predictor (CORT concentration) on host tolerance. The vertical axis is labelled on the response variable scale, effects are plotted on the scale of the linear predictor, and the results come from linear model regression model fitted with main effects of each cytokine and pre-inoculation CORT concentration.
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