PMC:7354481 / 5845-9095
Annnotations
{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7354481","sourcedb":"PMC","sourceid":"7354481","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7354481","text":"MicroRNAs (miRs) are non-coding RNAs of length approximately 20–22 nucleotides; they post-transcriptionally regulate gene expression by binding to the 3′-untranslated regions of target mRNAs, leading to degradation or translational inhibition. Each miR can target hundreds of mRNAs within a given cell type, and a single mRNA is often the target of multiple miRs, and thus over half of the human transcriptome is predicted to be under miR regulation, embedding this post-transcriptional control pathway within nearly every biological process [4,5]. Virally expressed miRs have recently been discovered, especially in viruses with DNA genomes. The best-known viral miRs are found mostly in herpesvirus families, where they enhance bilateral crosstalk between viral pathogenesis and host response mechanisms. Additionally, it has been shown that different virus families such as delta bovine leukaemia virus and foamy retroviruses could encode miRs [6]. As previously shown, viral miRs are critical in the immune evasion mechanisms, affecting host immunity-related gene regulation networks. This bilateral effect results in a rapid increase during the virus resistance against host defence mechanisms and leads to their survival in host cells [7]. The scope of miR generation from ssRNA viral genomes has been controversial, mainly due to the potentially deleterious effect of ssRNA viral genome cleavage into pre-/pri-miRs, making it unavailable for packaging into new virus particles. However, predictive studies on RNA viral genomes reveal RNA structures, which are conceivable Drosha and Dicer substrates. One of the well-described annotations was performed for HIV to define HIV-1 TAR RNA, a 59-nt long sequence that could generate a stem-loop structure similar to the pre-miR structure [8]. The identified numbers of viral miRs are not as many as for other organisms. One of the reasons for this is that viral miRs, due to their cytoplasmic location in host cells, render interaction with nuclear miR biogenesis elements of the host cells. Another hypothesis is that the cleavage of the viral RNA genome could generate miRs [9]. According to data obtained using in silico screening, there are fewer identified virus miRs compared with other species, and their functional roles in host cells are not well described. Therefore, greater effort is required to identify novel virally encoded miRs and to predict their host targets. Conversely, host cell miRs may alter the biological effect of the viruses [10]. Several interactions between viruses and the miRs in the host cells have been reported: the virus may either avoid being targeted by the cellular miRs [11]; block the cellular miRs to regulate key proteins in main signalling pathways [12,13]; synthesize their own viral miRs to create a more favourable cellular environment to survive in the host cells [14], or simply use the cellular miRs to their own advantage [15]. It should also be noted that host cell miR repertoires change dramatically in response to various diseases. Several underlying cardiovascular and lung conditions may significantly alter host miR expression, which would affect virus-host lung cell interactions, and may significantly determine the course of the 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