Date Published: October 19, 2018
Publisher: Public Library of Science
Author(s): Katherine E. Roberts, Jarrod D. Hadfield, Manmohan D. Sharma, Ben Longdon, David S. Schneider.
Host shifts–where a pathogen jumps between different host species–are an important source of emerging infectious disease. With on-going climate change there is an increasing need to understand the effect changes in temperature may have on emerging infectious disease. We investigated whether species’ susceptibilities change with temperature and ask if susceptibility is greatest at different temperatures in different species. We infected 45 species of Drosophilidae with an RNA virus and measured how viral load changes with temperature. We found the host phylogeny explained a large proportion of the variation in viral load at each temperature, with strong phylogenetic correlations between viral loads across temperature. The variance in viral load increased with temperature, while the mean viral load did not. This suggests that as temperature increases the most susceptible species become more susceptible, and the least susceptible less so. We found no significant relationship between a species’ susceptibility across temperatures, and proxies for thermal optima (critical thermal maximum and minimum or basal metabolic rate). These results suggest that whilst the rank order of species susceptibilities may remain the same with changes in temperature, some species may become more susceptible to a novel pathogen, and others less so.
Temperature is arguably the most important abiotic factor that affects all organisms, having both indirect and direct effects on physiology and life history traits [1–3]. There is much to be learned about the impact of climate change on infectious diseases [1,4,5]. Changes in temperature can impact both host and parasite biology, leading to complex and difficult to predict outcomes [2,6].
To investigate the effect of temperature on virus host shifts we quantified viral load in 12,827 flies over 396 biological replicates, from 45 species of Drosophilidae at three temperatures (Fig 1). DCV replicated in all host species, but viral load differed between species and temperatures (Fig 1). Species with similar viral loads cluster together on the phylogeny (Fig 2). Measurements were highly repeatable (Table 1), with a large proportion of the variance being explained by the inter-specific phylogenetic component (vp), with little within species or measurement error (vr) (Repeatability = vp/(vp + vr): Low = 0.90 (95% CI: 0.84, 0.95), Medium = 0.96 (95% CI: 0.93, 0.98), and High = 0.95, (95% CI: 0.89, 0.98)). We also calculated the proportion of between species variance that can be explained by the phylogeny as vp/(vp+ vs) , which is equivalent to Pagel’s lambda or phylogenetic heritability [69,72]. We found the host phylogeny explains a large proportion of the inter-specific variation in viral load across all three temperatures, although these estimates have broad confidence intervals due to the model struggling to separate the phylogenetic and non-phylogenetic components (Low = 0.77, 95% CI: 0.28, 0.99; Medium = 0.53, 95% CI: 0.31×10−5, 0.85; High = 0.40, 95% CI: 0.99×10−5, 0.74)
We found that susceptibilities of different species responded in different ways to changes in temperature. The susceptibilities of different species showed differing responses as temperatures increased (Fig 1). There was a strong phylogenetic correlation in viral load across the three experimental temperatures (Table 2). However, the variance in viral load increased with temperature, whereas the mean viral load did not show the same trend. This suggests that the rank order of susceptibility of the species remains relatively constant across temperatures, but as temperature increases the most susceptible species become more susceptible, and the least susceptible less so.