The viral genome controls viral replication (viral infection) within the host cell. Outside the host cell, in the released virus particle(virion), the genome is always surrounded by a protein envelope, the capsid. The virion represents the extracellular transport form for the transmission of the viral nucleic acid from one cell to another or from one host organism to another.
Errors in the replication of the genome occur mainly in viruses with an RNA genome. This is due to the fact that, in contrast to DNA-genomic viruses, the RNA-synthesizing enzymes (RNA polymerases) have no way of controlling the correctness of the newly synthesized strand. DNA-replicating enzymes (DNA polymerases) are capable of this control. In RNA replication processes, one building block is incorrectly incorporated for every103 -106 bases. In DNA replication processes, these read and insertion errors occur per108 -1011 bases, i.e. much less frequently. These mutations resulting from read errors form the basis for genetically distinct variants of a virus species. Many mutations are probably lethal for the virus and thus have no consequences for the infected organism and its environment. Others, however, fundamentally change their pathogenicity through the exchange of just one amino acid. Furthermore, the exchange of fragmented genomes (several pieces of nucleic acid form the complete genome) between viruses of the same species(reassortment ) also allows a high variability of genetic information. A typical example of this is given by the influenza virus.
Other viruses use the principle of so-called homologous recombination within a genomic segment. This mechanism is also possible in viruses with an unsegmented genome (e.g. coronaviruses) and is also used to create new virus types.