Herpes simplex virus 1 interaction with Toll-like receptor 2 contributes to lethal encephalitis.
By E. Kurt-Jones, M. Chan, Shenghua Zhou, Jennifer P. Wang, G. Reed, R. Bronson, M. Arnold, D. Knipe, R. Finberg. Proceedings of the National Academy of Sciences of the United States of America, 2004
656 citations recorded by the source corpus.
Subfields: Behavioral Neuroscience, Epidemiology, Immunology
View Paper: https://www.semanticscholar.org/paper/f9beb40b513dd9be2b9bd01fa85572774175daa8
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In Epidemiology
- T. Mogensen
- Masahiro Yamamoto
- Katherine A. Fitzgerald
- G. Trinchieri
- Shizuo Akira
- Taro Kawai
- R. Medzhitov
In Immunology
- Shizuo Akira
- T. Mogensen
- Katherine A. Fitzgerald
- A. Sher
- O. Takeuchi
- G. Trinchieri
- Masahiro Yamamoto
- R. Medzhitov
Citations in the corpus
- Cooperation of Toll-like receptor signals in innate immune defence (2007, background): “Similarly, Tlr2 −/− mice have decreased mortality when infected with herpes simplex virus 1 (HSV1), a phenotype that is attributed to the role of TLR2 in virus-induced encephaliti”
- Pathogen Recognition and Inflammatory Signaling in Innate Immune Defenses (2009, background): “The involvement of TLR-independent recognition systems in the early response to HSV infection has been strongly suggested by several individual reports (127, 223, 301) and further supported by in vivo data demonstrating that mice lacking TLR9 or myeloid differentiation primary-response gene 88 (MyD8”
- Toll-like receptors in antiviral innate immunity (2013, neutral): “In contrast, others found a detrimental role of TLR2 in HSV-1 infection, showing that TLR2 mediates a deregulated inflammatory response to the virus that contributes to lethal encephalitis [173,174].”
- The RNA Helicase Lgp2 Inhibits TLR-Independent Sensing of Viral Replication by Retinoic Acid-Inducible Gene-I1 (2005, background): “As a control for these measurements, we monitored the production of RANTES, another IRF-3-regulated gene, after SV infection, or stimulation by ligands for the following TLRs: poly(I-C) (TLR3), LPS (TLR4), R-848 (TLR7), and two other viruses, HSV-1 (TLR9) and influenza (TLR7).”
- Pathogen recognition and innate immunity. (2006, neutral): “It has been suggested that TLR2-mediated cytokine responses to HSV-1 are responsible for a significant portion of the morbidity and mortality associated with HSV-1 infection (Kurt-Jones et al., 2004).”