ArticleThe American journal of pathology2005
Lethal encephalitis in myeloid differentiation factor 88-deficient mice infected with herpes simplex virus 1.
Article in The American journal of pathology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
44 citing papers in PubMed, 90 citations in OpenAlex.
- Scratching the Surface Takes a Toll: Immune Recognition of Viral Proteins by Surface Toll-like Receptors.Viruses · 2022Review
- Microglia in antiviral immunity of the brain and spinal cord.Seminars in immunology · 2022Review
- Article
- When does hepatitis B virus meet long-stranded noncoding RNAs?Frontiers in microbiology · 2022Review
- Advancing Our Understanding of Corneal Herpes Simplex Virus-1 Immune Evasion Mechanisms and Future Therapeutics.Viruses · 2021Review
- Herpes simplex virus 1 targets IRF7 via ICP0 to limit type I IFN induction.Scientific reports · 2020Article
- Toll-like receptor-mediated innate immunity against herpesviridae infection: a current perspective on viral infection signaling pathways.Virology journal · 2020Review
- Herpes simplex encephalitis in adult patients with MASP-2 deficiency.PLoS pathogens · 2019Article
- Pathological processes activated by herpes simplex virus-1 (HSV-1) infection in the cornea.Cellular and molecular life sciences : CMLS · 2019Review
- Insights into the pathogenesis of herpes simplex encephalitis from mouse models.Mammalian genome : official journal of the International Mammalian Genome Society · 2018Review
- Dual TLR2/9 Recognition of Herpes Simplex Virus Infection Is Required for Recruitment and Activation of Monocytes and NK Cells and Restriction of Viral Dissemination to the Central Nervous System.Frontiers in immunology · 2018Article
- Herpes Simplex Virus Type 1 Engages Toll Like Receptor 2 to Recruit Macrophages During Infection of Enteric Neurons.Frontiers in microbiology · 2018Article
- Dendritic cells, macrophages, NK and CD8Virology journal · 2017Article
- MYD88 and functionally related genes are associated with multiple infections in a model population of Kenyan village dogs.Molecular biology reports · 2016Article
- p53 Is a Host Cell Regulator during Herpes Simplex Encephalitis.Journal of virology · 2016Article
- Article
- Myd88 Initiates Early Innate Immune Responses and Promotes CD4 T Cells during Coronavirus Encephalomyelitis.Journal of virology · 2015Article
- Prophylactic and therapeutic modulation of innate and adaptive immunity against mucosal infection of herpes simplex virus.Immune network · 2014Review
- Dual transcriptomics of virus-host interactions: comparing two Pacific oyster families presenting contrasted susceptibility to ostreid herpesvirus 1.BMC genomics · 2014Article
- Defense against HSV-1 in a murine model is mediated by iNOS and orchestrated by the activation of TLR2 and TLR9 in trigeminal ganglia.Journal of neuroinflammation · 2014Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Herpes simplex virus 1 (HSV-1), a large DNA virus from the Herpesviridae family, is the major cause of sporadic lethal encephalitis and blindness in humans. Recent studies have shown the importance of Toll-like receptors (TLRs) in the immune response to HSV-1 infection. Myeloid differentiation factor 88 (MyD88) is a critical adaptor protein that is downstream to mediated TLR activation and is essential for the production of inflammatory cytokines. Here, we studied the relationship between MyD88 and HSV-1 using a purified HSV-1 isolated from a natural oral recurrent human infection. We observed the activation of TLR-2 by HSV-1 in vitro using Chinese hamster ovary cells stably transfected with a reporter gene. Interestingly, we found that only peritoneal macrophages from MyD88-/- mice, but not macrophages from TRL2-/- or from wild-type mice, were unable to produce tumor necrosis factor-alpha in response to HSV-1 exposure. Additionally, although TLR2-/- mice showed no enhanced susceptibility to intranasal infection with HSV-1, MyD88-/- mice were highly susceptible to infection and displayed viral migration to the brain, severe neuropathological signs of encephalitis, and 100% mortality by day 10 after infection. Together, our results suggest that innate resistance to HSV-1 is mediated by MyD88 and may rely on activation of multiple TLRs.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.