Abstract
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.
Highlights
Virulence—the harm a pathogen does to its host—can be extremely high following a host shift, while other host shifts may go undetected as they cause few symptoms in the new host
Many emerging infectious diseases are the result of a host shift, with the pathogen jumping into the new host from another species
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
Summary
Virulence—which we define as the harm a pathogen does to its host—can sometimes dramatically increase when pathogens shift to infect new host species, resulting in new and devastating outbreaks and epidemics [1,2]. In bats, Ebola virus appears to be largely asymptomatic, but it is frequently fatal when it crosses the species barrier into humans and other primates [3,4]. Henipaviruses appear to be non-pathogenic in pteropoid bats, but can cause high levels of mortality in livestock and humans [5,6]. It was thought that novel host-parasite associations result in high levels of virulence and that long-term host-parasite interactions lead to the pathogen evolving towards avirulence [7]. Despite several high profile examples of host shifts resulting in extremely high virulence (see above), there may be a large ascertainment bias in detecting novel infections following hosts shifts, with only the most virulent likely to be detected and many benign infections going unnoticed [8]. It has been shown that long term coevolution does not necessarily lead to avirulence [9,10,11,12]
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