**1. Introduction**

Eight out of the hundred reported herpesviruses, from the family herpesviridae (herpein meaning, "to creep"), cause lytic and latent infections in the humans. The human herpesviruses are classified into the alpha-, beta- and the gamma-herpesviruses, based on the range of hosts they infect. The alpha (α)-herpesviruses, involving the herpes Simplex Virus −1 (HSV-1), HSV-2 and the varicella zoster virus (VZV), are known to infect a broad range of hosts while having a short replication cycle in these hosts. The beta (β)-herpesviruses include the members, the human cytomegalovirus (HCMV) and the reseolo-human herpesvirus −6 and − 7, and infect a restricted range of hosts as compared to the α-herpesviruses while having a longer replication cycle within these hosts. The third group known as the gamma (γ)- herpesviruses, containing the Epstein–Barr virus (EBV) and the Kaposi's sarcoma associated herpesvirus (KSHV), have the most restricted host range amongst the three sub-categories of human herpesviruses [1]. As reported for the year 2016, 13.2% of the global population aged 15 to 49 years were harboring HSV-2 within themselves, whereas about 66.6% amongst the 0 to 49 years aged individuals had HSV-1 infection [2]. Persons infected with HSV-2 are at 3 times to risk of infection with HIV compared to persons who are not infected with HSV-2 [3]. This may or

may not be due to a biological process as implied, but behavioral and the specific populations are vulnerable to infections with both the viruses. Both HSV-1 and 2 have an envelope of lipid-bilayer encasing them and have a double-stranded DNA (~152 kb) as their genetic material. The 12 glycoproteins in the outer layer participate in the entry of the HSV into the cell. The viral genes are expressed in an orderly fashion with the immediate early (IE) genes expressed first, which encode the proteins for the regulation of the viral replication. This is followed by the expression of the early (E) genes, which encode for the enzymes involved in the replication process. Finally, the expression of the late (L) genes takes place, which encode for the structural proteins of HSV [4]. The completion of the replicative cycle results in the generation of assembled virions which are transported via the endoplasmic reticulum/Golgi cargo transport system to the cell membrane, where the virions are released by acquiring a part of the host's cell membrane. HSV infection leads to pain and suffering, which although not always, may be lethal to the host. HSV-1 mainly causes the stromal keratitis in the eye whereas HSV-2 is responsible for genital lesions [4]. No vaccines against HSV are available for public use, although some are undergoing clinical trials. Therefore, drugs like Acyclovir, Valacyclovir and Famciclovir are the only therapeutic solutions available, which are associated with side-effects and limitations in bioavailability [5]. Thus, more suitable therapeutic agents, in terms of optimal bioavailability and diminished adverse effects, is the need of the hour.

MicroRNAs (miRNAs) on the other hand, are gaining a growing attention from the scientific community as the self-molecules which are the key regulators in infection and disease. These 20–24 nucleotides are non-protein coding RNAs which act post-transcriptionally to regulate the expression of the genes [6]. Since its discovery, miRNAs have found their significance in the diagnostics and therapeutics of diseases such as cancers, diabetes and infections of bacteria and viruses [7–13]. Thus, in this chapter, we have made an attempt to review the facts known about miRNAs are discuss their role in herpesvirus infection with our main focus on HSV infections.
