I have been studying endotoxin and its mechanisms lately, so I will post more on that soon. For now, I will just say that endotoxin seems to mediate most of its effects through the so-called TLR4 "receptor". In agreement with Peat's writings about flu and its connection to endotoxin, this study shows that the Dengue virus triggers the fever/shock through a protein that is an agonist/activator of the TLR4 "receptor". In other words, the Dengue fever is very much like the fever or shock that endotoxin itself causes. Blocking the TLR4 "receptor" completely stopped the Dengue fever. I wonder how many other viral "diseases", in addition to flu and Dengue, are simply an endotoxin "receptor" activation.
Niacinamide, cyproheptadine, mianserin, and methylene blue are some of the substances that can stop the endotoxin process and the associated fever and shock.
Viral Protein That Triggers Dengue Shock Identified
"...The team found that NS1 binds to Toll-like receptor 4 (TLR4), a molecule on the surface of immune cells known for recognizing and activating inflammatory responses against bacterial lipopolysaccharide (LPS), a component of bacterial cell membranes. When the researchers blocked TLR4 signaling with either a TLR4 antagonist or an anti-TLR4 antibody, the effect of NS1 on immune and endothelial cells was lost. Further experiments also showed that treatment with a TLR4 antagonist alleviated vascular leakage in a mouse model of dengue infection. This suggests that NS1 may act in manner similar to bacterial toxins such as LPS—by binding TLR4 and activating the production of inflammatory cytokines that then triggers vascular leakage. Indeed, the hallmarks of LPS-induced bacterial sepsis—increased production of inflammatory cytokines, increased vascular permeability, and subsequent septic shock—are uncannily similar to dengue-induced shock. Scientists are now interested in developing anti-dengue vaccines and drugs that target the NS1/TLR4 interaction. In a separate study published in the same issue of Science Translational Medicine, researchers led by Professor Eva Harris at the University of California, Berkeley found that immunizing mice with small amounts of NS1 protected them against subsequent lethal dengue infection. Such a vaccine, if developed, could prevent at-risk patients from progressing to severe dengue."
Niacinamide, cyproheptadine, mianserin, and methylene blue are some of the substances that can stop the endotoxin process and the associated fever and shock.
Viral Protein That Triggers Dengue Shock Identified
"...The team found that NS1 binds to Toll-like receptor 4 (TLR4), a molecule on the surface of immune cells known for recognizing and activating inflammatory responses against bacterial lipopolysaccharide (LPS), a component of bacterial cell membranes. When the researchers blocked TLR4 signaling with either a TLR4 antagonist or an anti-TLR4 antibody, the effect of NS1 on immune and endothelial cells was lost. Further experiments also showed that treatment with a TLR4 antagonist alleviated vascular leakage in a mouse model of dengue infection. This suggests that NS1 may act in manner similar to bacterial toxins such as LPS—by binding TLR4 and activating the production of inflammatory cytokines that then triggers vascular leakage. Indeed, the hallmarks of LPS-induced bacterial sepsis—increased production of inflammatory cytokines, increased vascular permeability, and subsequent septic shock—are uncannily similar to dengue-induced shock. Scientists are now interested in developing anti-dengue vaccines and drugs that target the NS1/TLR4 interaction. In a separate study published in the same issue of Science Translational Medicine, researchers led by Professor Eva Harris at the University of California, Berkeley found that immunizing mice with small amounts of NS1 protected them against subsequent lethal dengue infection. Such a vaccine, if developed, could prevent at-risk patients from progressing to severe dengue."