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In 2010, we described many similar DNA sequences in human and viral genomes, including herpesviral ones. The data obtained allowed us to suggest that these motifs may provide the antiviral protection by mating with a complementary potential target and destroying it by the catalytic way like small interfering RNA, siRNA. Since we have analyzed these viruses as a group, two major issues seemed to us curious: (1) the number of such motifs in genomes of various herpesvirus types, and (2) distribution of these motifs in an individual viral genome. Here we searched only the herpesviral genomes for short (>20 nt) continuous sequences (hits) that are totally identical to the sequences of human DNA. We found that different viral genes and genomes of different herpesviruses contain different amount of such hits. Assuming like in previous paper that the density of these hits in viral genes is associated with the probability to be targets for cellular siRNA, we consider the genomic allocation of this density as a hypothetical targetome map of the human herpesviruses. We combined all nine types of herpesviruses in the three groups according the hit concentration in their genomes and found that the resulting sequence corresponds to the type of cellular pathology caused by a virus. We do not assert now that this trend also relates to other human viruses or other viruses in general. As the GenBank continues to fill, it would be highly advisable to conduct further relevant research. We also suggested that a high hits concentration we found in the gene RL1 (ICP34.5) of the herpes simplex virus type 1 (HSV1) can make this gene a likely target for putative cellular endogenous siRNA. Artificial blockade of the gene RL1 attaches oncolytic properties to HSV1, and we do not exclude the possibility that part of the HSV1 population in humans with blocked RL1 in vivo, may participate in early anti-cancer protection during the reactivation of the virus from the latent state.

We describe a novel microarray-based approach for simultaneous identification and quantification of human immunodeficiency virus type 1 (HIV-1) and hepatitis B and C viruses (HBV and HCV) in donor plasma specimens. The method is based on multiplex real-time RT-PCR performed within the microarray hydrogel pads. Double-stranded amplification products are simultaneously detected using nonspecific SYBR Green I dye due to the reaction run in separate pads bearing 5′-immobilized specific primers. Both the sensitivity and specificity of the assay, based on 132 blood specimens analyzed, were 100% (56, 26, and 8 specimens were seropositive to HBV, HCV, and HIV-1, respectively; 22 were positive to both HIV-1 and HCV, and 2 positive to all three viruses; 18 samples were pathogen-negative). The dynamic range of the quantitative analysis covered a six-order interval ranging from 100 to 106 genome equivalents per assay. The 95% detection limits were 14 gEq for HIV-1, 10 gEq (1.7 IU) for HBV, and 15 gEq (7.5 IU) for HCV per assay. The proposed approach is considered to be versatile and could be adapted for simultaneous identification and quantification of numerous genetic targets.