**7. Mutational changes in virus genome and traceability**

As the inherent property of the virus genome, there is a higher mutational tendency compared to other micro/macro-organisms. The RNA virus replication does not comprise proofreading, as in the DNA cycle that this case renders genetic material to convenient for missing in the transcriptional phase [55]. This feature of RNA virus replication gives rise to high mutation possibility and formation of high yields, occurring of replication in a short time. RNA virus replication involves a complex and dynamic mutant formation ratio in certain genomic sites affecting the nucleotide sequence, caused by environmental factors. The model described for the evolution of virus shows comprehensible pathogenic behavior as quasispecies that have special population structure with a huge number of variant genomes relied on mutations [56]. These high mutation rates raised continually are changing in the relative frequency of the replication and selection. This process is the adoption of primitive replicons involving mutant distributions as seen in RNA viruses within their host [56, 57].

This mutational tendency depends on the population size of the virus involved in the infection. Therefore, a large population results in rapid fitness for cellular organisms. An important challenge in studies on RNA virus evolution is the differentiation, depending on phenotypic traits with ongoing specific mutations. They may associate different mutations with the biological behavior of the virus, which may be existence for the expression of phenotypic traits. These cases are the reason for the formation of restricted types. The findings on epidemiological, functional genomics, and structural studies showed the tolerance of the genetic changes on RNA viruses which are indispensable characteristic properties stemming from the virus evolution. However, the extinction of the viral infection cannot be estimated just from the characteristics of the existing sequence that is an unpredictable transitional phase of the genetic information based on lethal mutagenesis. Relied on the genomic data, the mutational ratio on viral sequences can be easily followed, but the effect of the mutation resulted in less epidemical and pathogenic behavior cannot be determined without clinical studies and monitoring on the host. Even the omics science provides predicational data on the virus, this is not enough alone if not supported by filiation studies on epidemic cases. This mutation limiting the pathogenicity of the virus may result in alternative solutions occurring spontaneously in nature for ending the viral infections.
