Evasion of Early Antiviral Responses by Herpes Simplex Viruses

Besides overcoming physical constraints, such as extreme temperatures, reduced humidity, elevated pressure, and natural predators, human pathogens further need to overcome an arsenal of antimicrobial components evolved by the host to limit infection, replication and optimally, reinfection. Herpes si...

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Main Authors: Paula A. Suazo, Francisco J. Ibañez, Angello R. Retamal-Díaz, Marysol V. Paz-Fiblas, Susan M. Bueno, Alexis M. Kalergis, Pablo A. González
Format: Article
Language:English
Published: Wiley 2015-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/2015/593757
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author Paula A. Suazo
Francisco J. Ibañez
Angello R. Retamal-Díaz
Marysol V. Paz-Fiblas
Susan M. Bueno
Alexis M. Kalergis
Pablo A. González
author_facet Paula A. Suazo
Francisco J. Ibañez
Angello R. Retamal-Díaz
Marysol V. Paz-Fiblas
Susan M. Bueno
Alexis M. Kalergis
Pablo A. González
author_sort Paula A. Suazo
collection DOAJ
description Besides overcoming physical constraints, such as extreme temperatures, reduced humidity, elevated pressure, and natural predators, human pathogens further need to overcome an arsenal of antimicrobial components evolved by the host to limit infection, replication and optimally, reinfection. Herpes simplex virus-1 (HSV-1) and herpes simplex virus-2 (HSV-2) infect humans at a high frequency and persist within the host for life by establishing latency in neurons. To gain access to these cells, herpes simplex viruses (HSVs) must replicate and block immediate host antiviral responses elicited by epithelial cells and innate immune components early after infection. During these processes, infected and noninfected neighboring cells, as well as tissue-resident and patrolling immune cells, will sense viral components and cell-associated danger signals and secrete soluble mediators. While type-I interferons aim at limiting virus spread, cytokines and chemokines will modulate resident and incoming immune cells. In this paper, we discuss recent findings relative to the early steps taking place during HSV infection and replication. Further, we discuss how HSVs evade detection by host cells and the molecular mechanisms evolved by these viruses to circumvent early antiviral mechanisms, ultimately leading to neuron infection and the establishment of latency.
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spelling doaj-art-54a9f698902740ff8068b622cbfdc95c2025-02-03T00:59:14ZengWileyMediators of Inflammation0962-93511466-18612015-01-01201510.1155/2015/593757593757Evasion of Early Antiviral Responses by Herpes Simplex VirusesPaula A. Suazo0Francisco J. Ibañez1Angello R. Retamal-Díaz2Marysol V. Paz-Fiblas3Susan M. Bueno4Alexis M. Kalergis5Pablo A. González6Millennium Institute on Immunology and Immunotherapy, Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, 8331010 Santiago, ChileMillennium Institute on Immunology and Immunotherapy, Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, 8331010 Santiago, ChileMillennium Institute on Immunology and Immunotherapy, Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, 8331010 Santiago, ChileMillennium Institute on Immunology and Immunotherapy, Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, 8331010 Santiago, ChileMillennium Institute on Immunology and Immunotherapy, Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, 8331010 Santiago, ChileMillennium Institute on Immunology and Immunotherapy, Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, 8331010 Santiago, ChileMillennium Institute on Immunology and Immunotherapy, Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, 8331010 Santiago, ChileBesides overcoming physical constraints, such as extreme temperatures, reduced humidity, elevated pressure, and natural predators, human pathogens further need to overcome an arsenal of antimicrobial components evolved by the host to limit infection, replication and optimally, reinfection. Herpes simplex virus-1 (HSV-1) and herpes simplex virus-2 (HSV-2) infect humans at a high frequency and persist within the host for life by establishing latency in neurons. To gain access to these cells, herpes simplex viruses (HSVs) must replicate and block immediate host antiviral responses elicited by epithelial cells and innate immune components early after infection. During these processes, infected and noninfected neighboring cells, as well as tissue-resident and patrolling immune cells, will sense viral components and cell-associated danger signals and secrete soluble mediators. While type-I interferons aim at limiting virus spread, cytokines and chemokines will modulate resident and incoming immune cells. In this paper, we discuss recent findings relative to the early steps taking place during HSV infection and replication. Further, we discuss how HSVs evade detection by host cells and the molecular mechanisms evolved by these viruses to circumvent early antiviral mechanisms, ultimately leading to neuron infection and the establishment of latency.http://dx.doi.org/10.1155/2015/593757
spellingShingle Paula A. Suazo
Francisco J. Ibañez
Angello R. Retamal-Díaz
Marysol V. Paz-Fiblas
Susan M. Bueno
Alexis M. Kalergis
Pablo A. González
Evasion of Early Antiviral Responses by Herpes Simplex Viruses
Mediators of Inflammation
title Evasion of Early Antiviral Responses by Herpes Simplex Viruses
title_full Evasion of Early Antiviral Responses by Herpes Simplex Viruses
title_fullStr Evasion of Early Antiviral Responses by Herpes Simplex Viruses
title_full_unstemmed Evasion of Early Antiviral Responses by Herpes Simplex Viruses
title_short Evasion of Early Antiviral Responses by Herpes Simplex Viruses
title_sort evasion of early antiviral responses by herpes simplex viruses
url http://dx.doi.org/10.1155/2015/593757
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