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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., Author summary Emerging infectious diseases are often the result of a host shift, where a pathogen jumps from one host species into another. Understanding the factors underlying host shifts is a major goal for infectious disease research. This effort has been further complicated by the fact that host-parasite interactions are now taking place in a period of unprecedented global climatic warming. Here, we ask how host shifts are affected by temperature by carrying out experimental infections using an RNA virus across a wide range of related species, at three different temperatures. We find that as temperature increases the most susceptible species become more susceptible, and the least susceptible less so. This has important consequences for our understanding of host shift events in a changing climate as it suggests that temperature changes may affect the likelihood of a host shift into certain species.

Emerging infectious diseases are often the result of a host shift, where the pathogen originates from a different host species. Virulence—the harm a pathogen does to its host—can be extremely high following a host shift (for example Ebola, HIV, and SARs), while other host shifts may go undetected as they cause few symptoms in the new host. Here we examine how virulence varies across host species by carrying out a large cross infection experiment using 48 species of Drosophilidae and an RNA virus. Host shifts resulted in dramatic variation in virulence, with benign infections in some species and rapid death in others. The change in virulence was highly predictable from the host phylogeny, with hosts clustering together in distinct clades displaying high or low virulence. High levels of virulence are associated with high viral loads, and this may determine the transmission rate of the virus., Author Summary Many emerging infectious diseases are the result of a host shift, with the pathogen jumping into the new host from another species. Virulence—the harm a pathogen does to its host—can be extremely high following a host shift (for example HIV, SARs and Ebola), while other host shifts may go undetected as they cause few symptoms in the new host. We have found that variation in virulence following host shifts can be extremely large and were highly predictable from the host phylogeny, with hosts clustering together in distinct clades displaying high or low virulence. These changes in virulence result from changes in viral load, and therefore the transmission potential of the virus. This suggests there is no clear rule to predict whether a pathogen will be virulent in a novel host. However, it does suggest a simple rule of thumb may be that if a pathogen causes high levels of virulence in any given host species, it will typically cause similar levels of virulence in closely related hosts.