Interaction between the cellular mRNA and the cellular microRNA linked to human immunodeficiency virus latency
Neil Tan Gana, Okamoto T.
Clin Vaccine Immunol. 2013(in press)
ABSTRACT: Although microRNAs (miR/s) play regulatory roles in a wide variety of cellular events, the regulatory mechanisms of miRs associated with viral diseases such as human immunodeficiency virus (HIV-1) infection, the causative agent of acquired immunodeficiency syndrome (AIDS), are largely unknown. In addition, the molecular mechanism of HIV viral latency is not fully understood. Thus, in order to understand the molecular mechanism of viral latency, we have attempted to clarify the role of cellular miR species that are upregulated in the maintenance of viral latency. Based on two previous reports and the data sets of the upregulated cellular miR upon HIV infection, we searched their target cellular mRNAs using an integrated ontology-based rich-text mining algorithm that enables the target identification of miRs. Using this algorithm we have identified four cellular gene modules namely: module 1 (cell cycle regulators) APOBEC7G, EIF5, MAPK, MYB, MYC, NCOA3, NKFB1, NFKBA1, P300, RAS, RAF, SRC1; module 2 (cell transcription factors) CREBBP, STAT1, STAT5A; module 3 (HIV-1 transcription modulators) RUNX1, TFCP2, YY1, and; module 4 (immune response genes) IFNA 1, IL15, IL6, IL2, IL7, IL10. A high stringency miR target analyses of the 3'-untranslated region (3'-UTR) sequences of these target genes identified common, and multiple in some cases, sequences within these modules. We have deciphered multiple gene regulatory networks using relational software STRINGS, which were consistent with previous observations. The findings clearly demonstrate the cross correlations between miR and mRNA in HIV infected cells.
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