Herpes viruses (simplex — for fever blisters, Kaposi’s sarcoma, herpes zoster — shingles) persist in the body in a latent state where they don’t don’t reproduce, don’t make many of their proteins and don’t make trouble. Every now and then they reproduce and cause disease, as anyone with recurrent fever blisters will tell you. Staying quiet allows them to avoid the immune system and essentially act as selfish DNA.
A recent paper [ PNAS vol. 120 e2212864120 ’23 ] shows that Kaposi’s Sarcoma Herpes Virus (KSHV) uses a circular RNA (circRNA) derived from a human oncogene called RELL1. The circular RNA they induce is called hsa_circ-0001400. In general circular RNAs are formed by back splicing of a 5′ splice to an upstream 3′ splice site. One of their functions is to act as sponges for microRNAs as some contain multiple binding sites for them. Some cells contain 25,000 of them.
Viruses are known to hijack cellular proteins to use for their own ends. It isn’t clear how the herpes viruses stimulate formation of hsa_circ_0001400, but use it they do, as it promotes viral latency, cell cycle genes and inhibits apoptosis.
This another example of the RNA world which supposedly existed before the DNA world, like DOS under the Windows operating system (forgotten but not gone)
Chemiotics II 