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Review
. 2011 Nov-Dec;1809(11-12):708-14.
doi: 10.1016/j.bbagrm.2011.06.012. Epub 2011 Jul 5.

Viral miRNAs and immune evasion

Affiliations
Review

Viral miRNAs and immune evasion

Isaac W Boss et al. Biochim Biophys Acta. 2011 Nov-Dec.

Abstract

Viral miRNAs, ~22nt RNA molecules which post-transcriptionally regulate gene expression, are emerging as important tools in immune evasion. Viral infection is a complex process that requires immune evasion in order to establish persistent life-long infection of the host. During this process viruses express both protein-coding and non-coding genes, which help to modulate the cellular environment making it more favorable for infection. In the last decade, it was uncovered that DNA viruses express a diverse and abundant pool of small non-coding RNA molecules, called microRNAs (miRNAs). These virally encoded miRNAs are non-immunogenic and therefore are important tools used to evade both innate and adaptive immune responses. This review aims to summarize our current knowledge of herpesvirus- and polyomavirus-encoded miRNAs, and how they contribute to immune evasion by targeting viral and/or host cellular genes. This article is part of a Special Issue entitled: MicroRNAs in viral gene regulation.

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Figures

Fig. 1
Fig. 1
Viral miRNAs can inhibit cell mediated immunity by modulating the recognition and activity of effector cells. (a) A CTL response to virally infected cells is initiated when the T-cell receptor (TCR) of CD8+T cells recognizes viral antigenic peptides presented by class I MHC molecules on the surface of infected cells. Viral miRNAs can block this initiating step by inhibiting the expression of viral peptides before they are presented. (b) NK cell killing of virally infected cells is initiated when an activation receptor (i.e. NKG2D) engages ligands (i.e. MICB or ULBP3) expressed by virally infected cells. Viral miRNAs can block this step by inhibiting the expression of these ligands. (c) Viral miRNAs can regulate the activities of leukocytes involved in the immune response by inhibiting the production of cytokines/chemokines which promote anti-viral immunity or by inducing production of cytokines that may inhibit anti-viral immunity.

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