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.

Fig 1. Viral loads of CrPV and DCV across DGRP lines during single and coinfection.

Bar heights show the mean viral load or changes in viral load (coinfection-single infection) at 2 dpi on a log₁₀ scale, with error bars showing the standard error of the mean. Blue bars represent single infection viral loads, or changes in viral load where single infection viral loads were greater than coinfection viral loads. Red bars represent coinfection viral loads, or changes in viral load where coinfection viral loads were greater than single infection viral loads. DGRP lines are arranged on the x-axis in order of susceptibility to CrPV during single infection.

Fig 2. Genetic correlations in viral load between single and coinfections of CrPV and DCV.

Correlations in viral load between CrPV during single and coinfection (A); DCV during single and coinfection (B); CrPV and DCV during single infection (C); and CrPV and DCV during coinfection (D). Individual points represent the mean viral load at 2 dpi for each DGRP line on a log₁₀ scale, with trend lines added from a univariate least-squares linear model for illustrative purposes. Genetic correlations (r), regression slopes (β), and 95% Cis have been taken from the output of model (1).

Fig 3. Viral loads of CrPV and DCV across host species during single and coinfection.

Bar heights show the mean viral load or changes in viral load (coinfection–single infection) by 2 dpi on a log₁₀ scale, with error bars showing the standard error of the mean. Blue bars represent single infection viral loads, or changes in viral load where single infection viral loads were greater than coinfection. Red bars represent coinfection viral loads, or changes in viral load where coinfection viral loads were greater than single infection. The phylogeny of Drosophilidae hosts is presented at the bottom, with the scale bar showing nucleotide substitutions per site, and the axis showing the approximate age since divergence in millions of years (mya) based on estimates from [91].

Fig 4. Interspecific correlations in viral load between single and coinfections of CrPV and DCV.

Correlations in viral load between CrPV during single and coinfection (A); DCV during single and coinfection (B); CrPV and DCV during single infection (C); and CrPV and DCV during coinfection (D). Individual points represent the mean viral load at 2dpi for each Drosophilidae host species on a log₁₀ scale, with trend lines added from a univariate least-squares linear model for illustrative purposes. Interspecific correlations (r), regression slopes (β), and 95% Cis have been taken from the output of model (4).