Abstract
Viral-derived elements and non-coding RNAs that build up “junk DNA” allow for flexible and context-dependent gene expression. They are extremely dense in the MHC region, accounting for flexible expression of the MHC I, II, and III genes and adjusting the level of immune response to the environmental stimuli. This review brings forward the viral-mediated aspects of the origin and evolution of adaptive immunity and aims to link this perspective with the MHC class I regulation. The complex regulatory network behind MHC expression is largely controlled by virus-derived elements, both as binding sites for immune transcription factors and as sources of regulatory non-coding RNAs. These regulatory RNAs are imbalanced in cancer and associate with different tumor types, making them promising targets for diagnostic and therapeutic interventions.
Highlights
Viruses are the most numerous and diverse agents in every habitat so far examined, and species-specific virus-derived information make up a substantial component of all organisms’ genomes and epigenomes [1,2,3,4,5]
Persistence is acquired via stable installation of the virus in the host cell by a mechanism described as an ‘addiction module’, where the killing effect of the virus is counter regulated by an anti-killing feature of the same virus and complemented by immune evasive viral mechanisms
In Eukaryotic cells, where the expression of genetic material is regulated by RNA-mediated processes, viral persistence is most often acquired via virus-encoded regulatory RNAs
Summary
Viruses are the most numerous and diverse agents in every habitat so far examined, and species-specific virus-derived information make up a substantial component of all organisms’ genomes and epigenomes [1,2,3,4,5]. Still the currently accepted perspective is that ERVs and their defectives are the remnants of past viral ‘plague sweeps’ retained in the genome of the surviving host, who cunningly co-opted them for structural and regulatory functions. This is the ‘host comes first’ perspective, which implies that point mutations and selection of the fittest type are sufficient to edit pre-existing code and assign it a new meaning (co-opt genes or regulators). We bring forward viral origins of adaptive immunity and review the current knowledge on MHC class I regulation by virus-derived elements.
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