Abstract
The awareness of viruses as a constant threat for human public health is a matter of fact and in this resides the need of understanding the mechanisms they use to trick the host. Viral non-coding RNAs are gaining much value and interest for the potential impact played in host gene regulation, acting as fine tuners of host cellular defense mechanisms. The implicit importance of v-ncRNAs resides first in the limited genomes size of viruses carrying only strictly necessary genomic sequences. The other crucial and appealing characteristic of v-ncRNAs is the non-immunogenicity, making them the perfect expedient to be used in the never-ending virus-host war. In this review, we wish to examine how DNA and RNA viruses have evolved a common strategy and which the crucial host pathways are targeted through v-ncRNAs in order to grant and facilitate their life cycle.
Highlights
Since 1964, when Epstein discovered, in pediatric cases of Burkitt’s lymphoma, the first human virus linked to malignancy, the scientific attention focused on the viral regulatory mechanisms within host cell capable to create the perfect cellular environment for viral replication
Many EBV-derived miRNA target genes involved in T cell polarization and migration, namely ebv-miR-BART1, -BART2, -BART10, -BART22, and -BHRF1, prevent the polarization of CD4+ T helper cells toward antiviral Th1 subtype acting on IL12B mRNA [36,38], whereas BHRF1-3 inhibits CXCL11 mRNA, blocking the chemotaxis of activated T cells [42]
In human B cells infected with KSHV, v-non-coding RNAs (ncRNAs) are mainly represented by nuclear polyadenylated (PAN) RNAs [98,99] that interact with demethylases JMJD3 and UTX [100]
Summary
Since 1964, when Epstein discovered, in pediatric cases of Burkitt’s lymphoma, the first human virus linked to malignancy, the scientific attention focused on the viral regulatory mechanisms within host cell capable to create the perfect cellular environment for viral replication. The eukaryotic cell, does not freely allow parasites to enter, so the viruses have developed many different mechanisms in order to skip the host cell barrage, beginning with the recognition of surface molecules acting as key door, and continuing with fundamental immune evasion, all aimed at translocating proteins and genetic material into the cells. On that note, it raises that viruses are not alive stricto sensu but, even if they are made of the simplest structure existent, they result the cleverest infectious agents because of the ability to adjust themselves, use and trick the host. We intent to examine how viruses have evolved a common strategy and which are the crucial host pathways targeted through v-ncRNAs in order to grant and facilitate their life cycle
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