Manipulation of Host Cell Death Pathways by Herpes Simplex Virus.

Manipulation of Host Cell Death Pathways by Herpes Simplex Virus. Curr Top Microbiol Immunol. 2020 Feb 15;: Authors: He S, Han J Abstract Herpes simplex virus (HSV)-1 and HSV-2 are ubiquitous human pathogens that infect keratinized epithelial surfaces and establish lifelong latent infection in sensory neurons of the peripheral nervous system. HSV-1 causes oral cold sores, and HSV-2 causes genital lesions characterized by recurrence at the site of the initial infection. In multicellular organisms, cell death plays a pivotal role in host defense by eliminating pathogen-infected cells. Apoptosis and necrosis are readily distinguished types of cell death. Apoptosis, the main form of programmed cell death, depends on the activity of certain caspases, a family of cysteine proteases. Necroptosis, a regulated form of necrosis that is unleashed when caspase activity is compromised, requires the activation of receptor-interacting protein (RIP) kinase 3 (RIPK3) through its interaction with other RIP homotypic interaction motif (RHIM)-containing proteins such as RIPK1. To ensure lifelong infection in the host, HSV carries out sophisticated molecular strategies to evade host cell death responses during viral infection. HSV-1 is a well-characterized pathogen that encodes potent viral inhibitors that modulate both caspase activation in the apoptosis pathway and RIPK3 activation in the necroptosis pathway in a dramatic, species-specific fashion. T...
Source: Current Topics in Microbiology and Immunology - Category: Microbiology Tags: Curr Top Microbiol Immunol Source Type: research