Pathological processes activated by herpes simplex virus-1 (HSV-1) infection in the cornea

Abstract

Herpes simplex virus type-1 (HSV-1) is a ubiquitous pathogen that infects a large majority of the human population worldwide. It is also a leading cause of infection-related blindness in the developed world. HSV-1 infection of the cornea begins with viral entry into resident cells via a multistep process that involves interaction of viral glycoproteins and host cell surface receptors. Once inside, HSV-1 infection induces a chronic immune-inflammatory response resulting in corneal scarring, thinning and neovascularization. This leads to development of various ocular diseases such as herpes stromal keratitis (HSK), resulting in visual impairment and eventual blindness. HSV-1 can also invade the central nervous system and lead to encephalitis, a relatively common cause of sporadic fetal encephalitis worldwide. In this review we discuss the pathological processes activated by corneal HSV-1 infection and existing anti-viral therapies as well as novel therapeutic options currently under development.

Intramuscular vaccination of mice with the human herpes simplex virus type-1(HSV-1) VC2 vaccine, but not its parental strain HSV-1(F) confers full protection against lethal ocular HSV-1 (McKrae) pathogenesis

“…HSV can cause a spectrum of disease including but not limited to primary and recurrent infections of mucous membranes such as gingivostomatitis, herpes labialis, and genital infections. They can also cause neonatal and congenital HSV infection, visceral HSV infections in immunocompromised hosts, and HSV encephalitis [6]. Ocular complications include lid, conjunctival, corneal, intraocular infections, and retinitis [5][6][7][8].…”

“…They can also cause neonatal and congenital HSV infection, visceral HSV infections in immunocompromised hosts, and HSV encephalitis [6]. Ocular complications include lid, conjunctival, corneal, intraocular infections, and retinitis [5][6][7][8]. Although HSV-2 is more restricted to infection of the genital epithelium [9], HSV-1 can cause infection on both genital and ocular areas [5,9].…”

Herpes Simplex Virus 1 MicroRNA miR-H28 Exported to Uninfected Cells in Exosomes Restricts Cell-to-Cell Virus Spread by Inducing Gamma Interferon mRNA

“…HSV-1 infects and establishes lifetime residence, in the form of latent infections, in nearly 100% of the human adult population (12)(13)(14). The most frequent form of transmission is by physical contact between small recurrent lesions induced by reactivation of latent virus and mucous membranes of uninfected individuals (15)(16)(17).…”

Transcription factor recruitment by parallel G-quadruplexes to promote transcription: the case of herpes simplex virus-1 ICP4

“…In particular, herpes simplex virus 1 (HSV-1) infects ~70% of the adult population, establishing a latent neuronal infection which, upon stressful conditions, may be reactivated to a lytic symptomatic state. HSV-1 is the major cause of blindness and viral encephalitis worldwide (Koujah et al, 2019). HSV-1 life cycle is characterized by a coordinated and sequential cascade of expression of three temporal classes of viral genes: the viral tegument protein VP16 prompts transcription of the immediate early (IE) viral genes, the products of which in turn activate transcription of the early (E) and late (L) viral genes; transcription of the late viral genes is also coupled to viral DNA replication (Dembowski and DeLuca, 2018).…”