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Programmed Cell Death-Dependent Host Defense in Ocular Herpes Simplex Virus Infection
Herpes simplex virus type 1 (HSV1) remains one of the most ubiquitous human pathogens on earth. The classical presentation of HSV1 infection occurs as a recurrent lesions of the oral mucosa commonly refer to as the common cold sore. However, HSV1 also is responsible for a range of ocular diseases in...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9023794/ https://www.ncbi.nlm.nih.gov/pubmed/35464953 http://dx.doi.org/10.3389/fmicb.2022.869064 |
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author | Guo, Hongyan Koehler, Heather S. Dix, Richard D. Mocarski, Edward S. |
author_facet | Guo, Hongyan Koehler, Heather S. Dix, Richard D. Mocarski, Edward S. |
author_sort | Guo, Hongyan |
collection | PubMed |
description | Herpes simplex virus type 1 (HSV1) remains one of the most ubiquitous human pathogens on earth. The classical presentation of HSV1 infection occurs as a recurrent lesions of the oral mucosa commonly refer to as the common cold sore. However, HSV1 also is responsible for a range of ocular diseases in immunocompetent persons that are of medical importance, causing vision loss that may result in blindness. These include a recurrent corneal disease, herpes stromal keratitis, and a retinal disease, acute retinal necrosis, for which clinically relevant animal models exist. Diverse host immune mechanisms mediate control over herpesviruses, sustaining lifelong latency in neurons. Programmed cell death (PCD) pathways including apoptosis, necroptosis, and pyroptosis serve as an innate immune mechanism that eliminates virus-infected cells and regulates infection-associated inflammation during virus invasion. These different types of cell death operate under distinct regulatory mechanisms but all server to curtail virus infection. Herpesviruses, including HSV1, have evolved numerous cell death evasion strategies that restrict the hosts ability to control PCD to subvert clearance of infection and modulate inflammation. In this review, we discuss the key studies that have contributed to our current knowledge of cell death pathways manipulated by HSV1 and relate the contributions of cell death to infection and potential ocular disease outcomes. |
format | Online Article Text |
id | pubmed-9023794 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-90237942022-04-23 Programmed Cell Death-Dependent Host Defense in Ocular Herpes Simplex Virus Infection Guo, Hongyan Koehler, Heather S. Dix, Richard D. Mocarski, Edward S. Front Microbiol Microbiology Herpes simplex virus type 1 (HSV1) remains one of the most ubiquitous human pathogens on earth. The classical presentation of HSV1 infection occurs as a recurrent lesions of the oral mucosa commonly refer to as the common cold sore. However, HSV1 also is responsible for a range of ocular diseases in immunocompetent persons that are of medical importance, causing vision loss that may result in blindness. These include a recurrent corneal disease, herpes stromal keratitis, and a retinal disease, acute retinal necrosis, for which clinically relevant animal models exist. Diverse host immune mechanisms mediate control over herpesviruses, sustaining lifelong latency in neurons. Programmed cell death (PCD) pathways including apoptosis, necroptosis, and pyroptosis serve as an innate immune mechanism that eliminates virus-infected cells and regulates infection-associated inflammation during virus invasion. These different types of cell death operate under distinct regulatory mechanisms but all server to curtail virus infection. Herpesviruses, including HSV1, have evolved numerous cell death evasion strategies that restrict the hosts ability to control PCD to subvert clearance of infection and modulate inflammation. In this review, we discuss the key studies that have contributed to our current knowledge of cell death pathways manipulated by HSV1 and relate the contributions of cell death to infection and potential ocular disease outcomes. Frontiers Media S.A. 2022-04-08 /pmc/articles/PMC9023794/ /pubmed/35464953 http://dx.doi.org/10.3389/fmicb.2022.869064 Text en Copyright © 2022 Guo, Koehler, Dix and Mocarski. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Microbiology Guo, Hongyan Koehler, Heather S. Dix, Richard D. Mocarski, Edward S. Programmed Cell Death-Dependent Host Defense in Ocular Herpes Simplex Virus Infection |
title | Programmed Cell Death-Dependent Host Defense in Ocular Herpes Simplex Virus Infection |
title_full | Programmed Cell Death-Dependent Host Defense in Ocular Herpes Simplex Virus Infection |
title_fullStr | Programmed Cell Death-Dependent Host Defense in Ocular Herpes Simplex Virus Infection |
title_full_unstemmed | Programmed Cell Death-Dependent Host Defense in Ocular Herpes Simplex Virus Infection |
title_short | Programmed Cell Death-Dependent Host Defense in Ocular Herpes Simplex Virus Infection |
title_sort | programmed cell death-dependent host defense in ocular herpes simplex virus infection |
topic | Microbiology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9023794/ https://www.ncbi.nlm.nih.gov/pubmed/35464953 http://dx.doi.org/10.3389/fmicb.2022.869064 |
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