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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Online Access: | http://dx.doi.org/10.1155/2015/593757 |
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doaj-54a9f698902740ff8068b622cbfdc95c2020-11-24T21:05:40ZengHindawi LimitedMediators 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 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Paula A. Suazo Francisco J. Ibañez Angello R. Retamal-Díaz Marysol V. Paz-Fiblas Susan M. Bueno Alexis M. Kalergis Pablo A. González |
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 |
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 |
title |
Evasion of Early Antiviral Responses by Herpes Simplex Viruses |
title_short |
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_sort |
evasion of early antiviral responses by herpes simplex viruses |
publisher |
Hindawi Limited |
series |
Mediators of Inflammation |
issn |
0962-9351 1466-1861 |
publishDate |
2015-01-01 |
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. |
url |
http://dx.doi.org/10.1155/2015/593757 |
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