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Toll-like receptor 4 in acute viral infection: Too much of a good thing
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Journal Article
Toll-like receptor 4 in acute viral infection: Too much of a good thing
2018
Overview
About the Authors: Judith Olejnik Affiliations Department of Microbiology, Boston University School of Medicine, Boston, Massachusetts, United States of America, National Emerging Infectious Diseases Laboratories, Boston University, Boston, Massachusetts, United States of America Adam J. Hume Affiliations Department of Microbiology, Boston University School of Medicine, Boston, Massachusetts, United States of America, National Emerging Infectious Diseases Laboratories, Boston University, Boston, Massachusetts, United States of America Elke Mühlberger * E-mail: muehlber@bu.edu Affiliations Department of Microbiology, Boston University School of Medicine, Boston, Massachusetts, United States of America, National Emerging Infectious Diseases Laboratories, Boston University, Boston, Massachusetts, United States of America ORCID logo http://orcid.org/0000-0003-3547-9376 Citation: Olejnik J, Hume AJ, Mühlberger E (2018) Toll-like receptor 4 in acute viral infection: Activation of TLR4 results in the recruitment of the intracellular adaptor protein, myeloid differentiation primary response 88 (MyD88), and/or toll/interleukin-1 receptor (TIR)-domain-containing adapter-inducing interferon-β (TRIF), ultimately resulting in the expression and secretion of pro-inflammatory mediators [6, 7]. [...]shed glycoprotein was detected at high levels in EBOV-infected guinea pigs, particularly shortly before death [34]. Respiratory syncytial virus fusion protein-induced toll-like receptor 4 (TLR4) signaling is inhibited by the TLR4 antagonists Rhodobacter sphaeroides lipopolysaccharide and eritoran (E5564) and requires direct interaction with MD-2.
Publisher
Public Library of Science,Public Library of Science (PLoS)
Subject
/ Analysis
/ Humans
/ Medicine
/ Medicine and Health Sciences
/ Pearls
/ Peptides
/ Proteins
/ TLR4
/ Toll-Like Receptor 4 - immunology
/ Viruses
