In silico prediction of cellular gene targets of herpesvirus encoded microRNAs
Afsar R. Naqvi,
Alexandra Seal,
Jennifer Shango,
Deepak Shukla,
Salvador Nares
Affiliations
Afsar R. Naqvi
Department of Periodontics, College of Dentistry, University of Illinois at Chicago, Chicago IL 60612 USA; Correspondence to: University of Illinois at Chicago, College of Dentistry, Department of Periodontics, 461A Dent MC 859, 801 South Paulina, Chicago, IL 60612, USA.
Alexandra Seal
Department of Periodontics, College of Dentistry, University of Illinois at Chicago, Chicago IL 60612 USA
Jennifer Shango
Department of Periodontics, College of Dentistry, University of Illinois at Chicago, Chicago IL 60612 USA
Deepak Shukla
Department of Microbiology and Immunology, University of Illinois at Chicago, Chicago, IL, 60612, USA; Department of Ophthalmology and Visual Sciences, University of Illinois Medical Center, Chicago, IL, 60612, USA
Salvador Nares
Department of Periodontics, College of Dentistry, University of Illinois at Chicago, Chicago IL 60612 USA; Correspondence to: University of Illinois at Chicago, College of Dentistry, Department of Periodontics, 458 Dent MC 859, 801 South Paulina, Chicago, IL 60612, USA.
Herpesviruses have evolved to encode multiple microRNAs [viral miRNAs (v-miRs)], a unique feature of this family of double stranded DNA (dsDNA) viruses. However, functional role of these v-miRs in host-pathogen interaction remains poorly studied. In this data, we examined the impact of oral disease associated v-miRs viz., miR-H1 [encoded by herpes simplex virus 1 (HSV1)] and miR-K12-3 [encoded by Kaposi sarcoma-associated herpesvirus (KSHV)] by identifying putative targets of viral miRNAs. We used our published microarray data (GSE107005) to identify the transcripts downregulated by the v-miRs. The 3′ untranslated region (UTR) of these genes were extracted using BioMart tool on Ensembl and subjected to RNA:RNA interaction employing RNA Hybrid. We obtained hundreds of potential and novel miR-H1 and miR-K12-3 binding sites on the 3′UTR of the genes downregulated by these v-miRs. The information can provide likely regulatory mechanisms of the candidate v-miRs through which they can exert biological impact during herpesvirus infection and pathogenesis.
