Impact of Toll-Like Receptors (TLRs) and TLR Signaling Proteins in Trigeminal Ganglia Impairing Herpes Simplex Virus 1 (HSV-1) Progression to Encephalitis: Insights from Mouse Models
Herpes simplex virus 1 (HSV-1) or simplexvirus humanalpha 1 is a neurotropic virus that is responsible for orofacial infections in humans. More than 70% of the world’s population may have seropositivity for HSV-1, and this virus is a leading cause of sporadic lethal encephalitis in humans. The role...
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IMR Press
2024-03-01
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Series: | Frontiers in Bioscience-Landmark |
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Online Access: | https://www.imrpress.com/journal/FBL/29/3/10.31083/j.fbl2903102 |
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author | Marco Antônio Campos Guilherme de Pádua Zolini Erna Geessien Kroon |
author_facet | Marco Antônio Campos Guilherme de Pádua Zolini Erna Geessien Kroon |
author_sort | Marco Antônio Campos |
collection | DOAJ |
description | Herpes simplex virus 1 (HSV-1) or simplexvirus humanalpha 1 is a neurotropic virus that is responsible for orofacial infections in humans. More than 70% of the world’s population may have seropositivity for HSV-1, and this virus is a leading cause of sporadic lethal encephalitis in humans. The role of toll-like receptors (TLRs) in defending against HSV-1 infection has been explored, including the consequences of lacking these receptors or other proteins in the TLR pathway. Cell and mouse models have been used to study the importance of these receptors in combating HSV-1, how they relate to the innate immune response, and how they participate in the orchestration of the adaptive immune response. Myeloid differentiation factor 88 (MyD88) is a protein involved in the downstream activation of TLRs and plays a crucial role in this signaling. Mice with functional MyD88 or TLR2 and TLR9 can survive HSV-1 infection. However, they can develop encephalitis and face a 100% mortality rate in a dose-dependent manner when MyD88 or TLR2 plus TLR9 proteins are non-functional. In TLR2/9 knockout mice, an increase in chemokines and decreases in nitric oxide (NO), interferon (IFN) gamma, and interleukin 1 (IL-1) levels in the trigeminal ganglia (TG) have been correlated with mortality. |
first_indexed | 2024-04-24T17:39:04Z |
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issn | 2768-6701 |
language | English |
last_indexed | 2024-04-24T17:39:04Z |
publishDate | 2024-03-01 |
publisher | IMR Press |
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series | Frontiers in Bioscience-Landmark |
spelling | doaj.art-f300cd569014478e95ba582d16e2d1ab2024-03-28T02:27:54ZengIMR PressFrontiers in Bioscience-Landmark2768-67012024-03-0129310210.31083/j.fbl2903102S2768-6701(24)01187-0Impact of Toll-Like Receptors (TLRs) and TLR Signaling Proteins in Trigeminal Ganglia Impairing Herpes Simplex Virus 1 (HSV-1) Progression to Encephalitis: Insights from Mouse ModelsMarco Antônio Campos0Guilherme de Pádua Zolini1Erna Geessien Kroon2Imunologia de Doenças Virais, Instituto René Rachou, Fundação Oswaldo Cruz, 30190-002 Belo Horizonte, MG, BrazilDepartamento de Vigilância Sanitária, Secretaria Municipal de Saúde de Varginha, 37010-600 Varginha, MG, BrazilLaboratório de Vírus, Departamento de Microbiologia, Instituto de Ciências Biológicas (ICB), Universidade Federal de Minas Gerais (UFMG), 31270-901 Belo Horizonte, MG, BrazilHerpes simplex virus 1 (HSV-1) or simplexvirus humanalpha 1 is a neurotropic virus that is responsible for orofacial infections in humans. More than 70% of the world’s population may have seropositivity for HSV-1, and this virus is a leading cause of sporadic lethal encephalitis in humans. The role of toll-like receptors (TLRs) in defending against HSV-1 infection has been explored, including the consequences of lacking these receptors or other proteins in the TLR pathway. Cell and mouse models have been used to study the importance of these receptors in combating HSV-1, how they relate to the innate immune response, and how they participate in the orchestration of the adaptive immune response. Myeloid differentiation factor 88 (MyD88) is a protein involved in the downstream activation of TLRs and plays a crucial role in this signaling. Mice with functional MyD88 or TLR2 and TLR9 can survive HSV-1 infection. However, they can develop encephalitis and face a 100% mortality rate in a dose-dependent manner when MyD88 or TLR2 plus TLR9 proteins are non-functional. In TLR2/9 knockout mice, an increase in chemokines and decreases in nitric oxide (NO), interferon (IFN) gamma, and interleukin 1 (IL-1) levels in the trigeminal ganglia (TG) have been correlated with mortality.https://www.imrpress.com/journal/FBL/29/3/10.31083/j.fbl2903102hsv-1tlr-induced immune responseencephalitisdefective tlrinnate immunity |
spellingShingle | Marco Antônio Campos Guilherme de Pádua Zolini Erna Geessien Kroon Impact of Toll-Like Receptors (TLRs) and TLR Signaling Proteins in Trigeminal Ganglia Impairing Herpes Simplex Virus 1 (HSV-1) Progression to Encephalitis: Insights from Mouse Models Frontiers in Bioscience-Landmark hsv-1 tlr-induced immune response encephalitis defective tlr innate immunity |
title | Impact of Toll-Like Receptors (TLRs) and TLR Signaling Proteins in Trigeminal Ganglia Impairing Herpes Simplex Virus 1 (HSV-1) Progression to Encephalitis: Insights from Mouse Models |
title_full | Impact of Toll-Like Receptors (TLRs) and TLR Signaling Proteins in Trigeminal Ganglia Impairing Herpes Simplex Virus 1 (HSV-1) Progression to Encephalitis: Insights from Mouse Models |
title_fullStr | Impact of Toll-Like Receptors (TLRs) and TLR Signaling Proteins in Trigeminal Ganglia Impairing Herpes Simplex Virus 1 (HSV-1) Progression to Encephalitis: Insights from Mouse Models |
title_full_unstemmed | Impact of Toll-Like Receptors (TLRs) and TLR Signaling Proteins in Trigeminal Ganglia Impairing Herpes Simplex Virus 1 (HSV-1) Progression to Encephalitis: Insights from Mouse Models |
title_short | Impact of Toll-Like Receptors (TLRs) and TLR Signaling Proteins in Trigeminal Ganglia Impairing Herpes Simplex Virus 1 (HSV-1) Progression to Encephalitis: Insights from Mouse Models |
title_sort | impact of toll like receptors tlrs and tlr signaling proteins in trigeminal ganglia impairing herpes simplex virus 1 hsv 1 progression to encephalitis insights from mouse models |
topic | hsv-1 tlr-induced immune response encephalitis defective tlr innate immunity |
url | https://www.imrpress.com/journal/FBL/29/3/10.31083/j.fbl2903102 |
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