Investigating the outcomes of virus coinfection within and across host species

Abstract

Interactions between coinfecting pathogens have the potential to alter the course of infection and can act as a source of phenotypic variation in susceptibility between hosts. This phenotypic variation may influence the evolution of host-pathogen interactions within host species and interfere with patterns in the outcomes of infection across host species. Here, we examine experimental coinfections of two Cripaviruses–Cricket Paralysis Virus (CrPV), and Drosophila C Virus (DCV)–across a panel of 25 Drosophila melanogaster inbred lines and 47 Drosophilidae host species. We find that interactions between these viruses alter viral loads across D. melanogaster genotypes, with a ~3 fold increase in the viral load of DCV and a ~2.5 fold decrease in CrPV in coinfection compared to single infection, but we find little evidence of a host genetic basis for these effects. Across host species, we find no evidence of systematic changes in susceptibility during coinfection, with no interaction between DCV and CrPV detected in the majority of host species. These results suggest that phenotypic variation in coinfection interactions within host species can occur independently of natural host genetic variation in susceptibility, and that patterns of susceptibility across host species to single infections can be robust to the added complexity of coinfection. The susceptibility of a host to infection can be influenced by the presence of co-occurring (i.e., coinfecting) pathogens, which can interact by suppressing and activating host immunity, and competing for host resources. The influence of coinfections on host susceptibility could have ramifications for the evolution of hosts and pathogens, and this may be seen within a single host species as a change in the contribution of host genetics to susceptibility during coinfections, and across host species as a change in the ability of evolutionary relationships to explain similarities in susceptibility. Here, we test these possibilities by measuring susceptibility to two different Cripaviruses during single infections and coinfections across different insect host genotypes and host species. We find that these two viruses interact during coinfections within the fruit fly Drosophila melanogaster, altering host susceptibility, but that variation in this interaction didn’t show any evidence of being influenced by host genetics. Similarly, we find little evidence of the explanatory power of evolutionary relationships across host species changing between single infections and coinfections. These results suggest that variation in interactions between pathogens can occur without the influence of host genetics, and that it is possible for patterns in susceptibility across host species measured during single infection to be maintained during coinfection.