In general, the action of viruses and mobile genetic elements is important in host evolution [ 16, 42- 47] because they are vectors of evolution and potential inducers of diseases and genetic disorders, such as chromosome rearrangements and inversions [ 48].
However, if the action of viruses and mobile genetic elements might somehow influence the host evolution, it is reasonable that host evolution could also constrain the evolution of these genetic agents.
The constant formation of DNA microsatellites through slippage by the replication machinery, and the action of viruses and transposons, also complicate the word landscape, especially in regions with lower selective constraints (such as introns, UTRs and intergenic regions) [ 6, 7].
To test whether such potential 'hot spots' of immune system evolution are a general phenomenon will require data from a wider range of invertebrate taxa, and based on sequence analysis alone it will remain hard to attribute selection to the action of viruses.
The overall composition of vsiRNAs and satsiRNAs in the infected plants reflect the combined action of virus, satRNA and different DCLs in host plants.
Many of these processes require action of virus-encoded signals and cellular proteins.
These should inhibit formation of virus structural and nonstructural envelope proteins and can suppress the lethal action of virus generated molecules.
Temporal relationship between viral and bacterial infections has been observed, and may arise via the action of virus-induced inflammatory cytokines.
The actions of the virus depend both on its destructive tendencies toward a specific host cell and on environmental conditions.
In particular, is there any strong evidence of the assumed heterogeneity of tumor cell populations with regard to killing action of oncolytic viruses, and does this assumption improve the quality of the model and its predictive power?
The hypothesis that tumor cell populations are heterogeneous with regard to the killing action of oncolytic viruses is a general one, and our model strongly suggests that the assumption of homogeneity (that is, that all the tumor cells behave in the same way under oncolytic virus infection) is an oversimplification.
