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Viruses and their hosts are involved in an 'arms race' where they continuallyevolve mechanisms to overcome each other. It has long been proposed thatintrinsic disorder provides a substrate for the evolution of viral hijackfunctions and that short linear motifs (SLiMs) are important players in thisprocess. Here, we review evidence in support of this tenet from two modelsystems: the papillomavirus E7 protein and the adenovirus E1A protein.Phylogenetic reconstructions reveal that SLiMs appear and disappear multipletimes across evolution, providing evidence of convergent evolution withinindividual viral phylogenies. Multiple functionally related SLiMs show strongco-evolution signals that persist across long distances in the primary sequenceand occur in unrelated viral proteins. Moreover, changes in SLiMs areassociated with changes in phenotypic traits such as host range and tropism.Tracking viral evolutionary events reveals that host switch events areassociated with the loss of several SLiMs, suggesting that SLiMs are underfunctional selection and that changes in SLiMs support viral adaptation.Fine-tuning of viral SLiM sequences can improve affinity, allowing them tooutcompete host counterparts. However, viral SLiMs are not always competitiveby themselves, and tethering of two suboptimal SLiMs by a disordered linker mayinstead enable viral hijack. Coevolution between the SLiMs and the linkerindicates that the evolution of disordered regions may be more constrained thanpreviously thought. In summary, experimental and computational studies supporta role for SLiMs and intrinsic disorder in viral hijack functions and in viraladaptive evolution.

Evolution of SLiM-mediated hijack functions in intrinsically disordered viral proteins