Wow Ohm, that is really interesting. Thank you for pointing that out. I am trying to better understand the differences between the CCR5 inhibitors.
Do you per chance know if maraviroc has a similar effect on MCP-1 given that it's also a small molecule blocker?
I think this article describing the synergism between RANTES and MCP-1 when it comes to pulmonary inflammation might substantiate what you are saying about it not being good, especially when it comes to COVID and inflammation in the lungs.
MCP-1 and RANTES are mediators of acute and chronic inflammation
Abstract
One last question, as I have seen some back and forth on twitter about this. Do you have an opinion on the liver toxicity issues of maraviroc if shorter duration doses are given (i.e weeks for COVID vs. years for HIV)? Do you subscribe to the risk of the black box warning being reduced/eliminated?
As always, thanks in advance for helping us armchair scientists wrap our head around things!
Do you per chance know if maraviroc has a similar effect on MCP-1 given that it's also a small molecule blocker?
I think this article describing the synergism between RANTES and MCP-1 when it comes to pulmonary inflammation might substantiate what you are saying about it not being good, especially when it comes to COVID and inflammation in the lungs.
MCP-1 and RANTES are mediators of acute and chronic inflammation
Abstract
Quote:Regulation of leukocyte migration and activation by chemokines are recognized as potentially important functions in the induction of acute and chronic inflammatory reactions. Regulated upon activation normal T cell expressed and presumably secreted (RANTES), monocyte chemotactic protein-1 (MCP-1), and related molecules constitute the C-C class of the beta chemokine supergene family with inflammatory properties. Here we report that in experimental studies RANTES and MCP-1 provoke mast cell activation and increase histidine decarboxylase mRNA expression in a dose-dependent manner. Moreover, injections of RANTES and MCP-1 in the rat skin cause mast cell, eosinophil, and macrophage recruitment, and prostaglandin E2 (PGE2) generation. In a chronic inflammatory model MCP-1 was found to mediate the recruitment of mononuclear cells in calcified granulomas. In addition, MCP-1 mediated parasitic infections caused by Trichinella spiralis. In accordance with other studies, RANTES and MCP-1 were found to play an important role in the lung allergic inflammation, lung leukocyte infiltration, bronchial hyperresponsiveness, and the recruitment of eosinophils in the pathogenesis of asthma. Here for the first time we propose a new mechanism of pulmonary airway inflammation where RANTES and MCP-1 are deeply involved. We also studied the apparent role played by RANTES in the pathogenesis of relapsing-remitting multiple sclerosis enhancing the inflammatory response within the nervous system.
One last question, as I have seen some back and forth on twitter about this. Do you have an opinion on the liver toxicity issues of maraviroc if shorter duration doses are given (i.e weeks for COVID vs. years for HIV)? Do you subscribe to the risk of the black box warning being reduced/eliminated?
As always, thanks in advance for helping us armchair scientists wrap our head around things!
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