Abstract
Non-coding RNAs, particularly lncRNAs and miRNAs, have recently been shown to regulate different steps in viral infections and induction of immune responses against viruses. Expressions of several host and viral lncRNAs have been found to be altered during viral infection. These lncRNAs can exert antiviral function via inhibition of viral infection or stimulation of antiviral immune response. Some other lncRNAs can promote viral replication or suppress antiviral responses. The current review summarizes the interaction between ncRNAs and herpes simplex virus, cytomegalovirus, and Epstein–Barr infections. The data presented in this review helps identify viral-related regulators and proposes novel strategies for the prevention and treatment of viral infection.
Highlights
The human genome consists of a variety of non-protein-coding DNA
While long ncRNAs (lncRNAs) regulate gene expression at different levels, miRNAs mainly act at a post-transcriptional level
We summarize the interaction between non-coding RNAs (ncRNAs) and herpes simplex virus (HSV), cytomegalovirus (CMV), and Epstein–Barr (EBV) infections
Summary
The human genome consists of a variety of non-protein-coding DNA. A proportion of these genomic regions are transcribed into RNA. Kaposi’s sarcoma-associated HSV encodes a viral oncogene, namely, viral interferon regulatory factor 1 (vIRF1) This oncogene enhances migration potential and aggressiveness of endothelial cells through decreasing expression of miR-218-5p to release its targets. HSV-1 has been shown to encode miR-H2-3p, a miRNA that interferes with cytosolic DNA-induced antiviral innate immune responses through decreasing expression of DEAD-Box Helicase 41 (DDX41) [16]. ARFGEF1 increases cell motility, invasion, proliferation, and angiogenesis in Kaposi’s sarcoma-associated herpesvirus infected cells This miRNA induces improved levels of viral replication and gene expression by regulating. DDX41, IFN-β, MxI miR-H2-3p lowers innate immune response in infected cells and intensifies viral DNA replication and proliferation This miRNA is encoded by gamma-herpesviruses and is a necessary factor for its infection and splenic latency.
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
