Abstract
Understanding biological mechanisms that regulate emergence of viral diseases, in particular those events engaging cross-species pathogens spillover, is becoming increasingly important in virology. Species barrier jumping has been extensively studied in animal viruses, and the critical role of a suitable intermediate host in animal viruses-generated human pandemics is highly topical. However, studies on host jumping involving plant viruses have been focused on shifting intra-species, leaving aside the putative role of “bridge hosts” in facilitating interspecies crossing. Here, we take advantage of several VPg mutants, derived from a chimeric construct of the potyvirus Plum pox virus (PPV), analyzing its differential behaviour in three herbaceous species. Our results showed that two VPg mutations in a Nicotiana clevelandii-adapted virus, emerged during adaptation to the bridge-host Arabidopsis thaliana, drastically prompted partial adaptation to Chenopodium foetidum. Although both changes are expected to facilitate productive interactions with eIF(iso)4E, polymorphims detected in PPV VPg and the three eIF(iso)4E studied, extrapolated to a recent VPg:eIF4E structural model, suggested that two adaptation ways can be operating. Remarkably, we found that VPg mutations driving host-range expansion in two non-related species, not only are not associated with cost trade-off constraints in the original host, but also improve fitness on it.
Highlights
Emerging viral diseases are frequently the result of host jumps, when a pathogen gains the ability to infect a new species [1,2]
In order to examine whether the detected changes at VPg sequence are solely responsible for the gain of infectivity, we assayed the effect of these mutations, proline to serine at position 114 (P114S) and phenylalanine to serine at position 163 (F163L), separately engineered into the cDNA clone of the Plum pox virus (PPV)-VPgSwCM-R chimera
The ratio of the DNA inoculum was reversed in two of the analyzed pools, and the double mutant, despite its lesser initial representation, became the majority virus (Figure 2). These results suggest that the enhancement of viral fitness in A. thaliana conferred by the F163L mutation in the VPg of PPV-SwCMp might be greater than that provided by the P114S mutation
Summary
Emerging viral diseases are frequently the result of host jumps, when a pathogen gains the ability to infect a new species [1,2]. Host jumping has received particular attention in the case of animal and human diseases, with the host range breadth being a major determinant of bacterial and viral emerging outbreaks [3,4,5]. Viral host jumping goes hand in hand with the concept of adaptive trade-off, according to which a pathogen cannot simultaneously maximize its fitness in all hosts. Viral adaptation to a particular species normally implies a fitness cost in alternative species, and generalist viruses infecting numerous hosts evolve to reach fitness values maximized among hosts, but lower than the optimum they would have reached if had adapted to a single host [12]
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