In 2015, we described short continuous fragments of human herpesvirus DNA, identical to the cellular ones, which we called microhomology (hits) because of their small size (≥ 20 nt). We noticed that generally the increase in the density (D) of these hits in human herpesviruses is inversely proportional to a decrease in the pathogenicity of these viruses. In this small work, we are considering the question of the existence of more objective features of HHV DNA (which can accompany the dynamics of the density of hits from HHV5 to HHV7), rather than a very imprecise notion of the degree of pathogenicity of a viral infection.

We show here that D really correlates with certain formal parameters of HHV DNA, primarily with their macrostructure, that is, with the number of segments of the HV genomes, their isomerization and size. According to these parameters, herpesvirus DNA can be divided into three groups, not strictly coinciding with the classification by subfamilies, genera and species. For a more detailed division (on species and strain level) according to the formal parameters discussed here and more convincing conclusions on the basis of the microhomology density between the viral and the host genomes, the number of completely sequenced HV DNAs is not enough for today. The situation is exacerbated by the low density of hits in the HV genome (5-20%) and their possible ambiguous functions. Some of the hits may have functional significance, as we suggested earlier [1,2], another part may be an accidental consequence of the close interaction of the viral and cellular genomes, for some reason fixed by selection. Nevertheless, the options for solving the task can be identified today.