Filatov F, Shargunov A (2018) Microhomology of Viral/Host DNAs and Macrostructure of Herpesviral Genome. Int J Virol AIDS 5:042.


© 2018 Filatov F, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

RESEARCH ARTICLE | OPEN ACCESS DOI: 10.23937/2469-567X/1510042

Microhomology of Viral/Host DNAs and Macrostructure of Herpesviral Genome

Felix Filatov1,2* and Alexandr Shargunov1

1Mechnikov Federal Research Institute of Vaccines and Sera, Moscow, Russia

2Gamaleya Federal Research Center of Epidemiology and Microbiology, Moscow, Russia


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.