title: Autophagy interaction with herpes simplex virus type-1 infection.
abstract: More than 50% of the U.S. population is infected with herpes simplex virus type-I (HSV-1) and global infectious estimates are nearly 90%. HSV-1 is normally seen as a harmless virus but debilitating diseases can arise, including encephalitis and ocular diseases. HSV-1 is unique in that it can undermine host defenses and establish lifelong infection in neurons. Viral reactivation from latency may allow HSV-1 to lay siege to the brain (Herpes encephalitis). Recent advances maintain that HSV-1 proteins act to suppress and/or control the lysosome-dependent degradation pathway of macroautophagy (hereafter autophagy) and consequently, in neurons, may be coupled with the advancement of HSV-1-associated pathogenesis. Furthermore, increasing evidence suggests that HSV-1 infection may constitute a gradual risk factor for neurodegenerative disorders. The relationship between HSV-1 infection and autophagy manipulation combined with neuropathogenesis may be intimately intertwined demanding further investigation.
authors.affiliation: a Department of Molecular Microbiology and Immunology , Keck Medical School, University of Southern California , Los Angeles , CA , USA.
authors.forename: Douglas
authors.initials: D
authors.lastname: O'Connell
authors.affiliation: a Department of Molecular Microbiology and Immunology , Keck Medical School, University of Southern California , Los Angeles , CA , USA.
authors.forename: Chengyu
authors.initials: C
authors.lastname: Liang
mesh_terms: D001343:Autophagy; D006561:Herpes Simplex / Q000473:pathology* / Q000821:virology*; D018259:Herpesvirus 1, Human / Q000502:physiology*; D006801:Humans; D009410:Nerve Degeneration / Q000473:pathology / Q000821:virology; D009474:Neurons / Q000473:pathology; D012307:Risk Factors
keywords: ICP34.5; autophagy; herpes simplex virus; immune evasion; neurodegeneration