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Wednesday, June 10, 2020 12:17:58 PM
The reason I am interested in this particular question is because my working hypothesis is that, for the most part, the immune system knows what it is doing.
In someone with a normal immune system the immune response is always an over-response. The body wants to take care of the immediate threat even if it causes pain and suffering. Thus 51 diseases on the leronlimab disease list.
Also, they do not demonstrate that the inflammation in a cold (sore throat, runny nose) is the result of immune system overreaction; they hypothesize that it is overreaction because they were impressed by how many chemicals were involved: why would there be so many chemicals involved in such a non-serious infection?
You don't seem to be aware of the interconnectivity of the entire immune system or why inflammation develops.
They list a bunch of chemicals that they noted were upregulated in rhinovirus infection. RANTES (CCL5) and IL-6 were not mentioned. Dr. Patterson's paper did not show much change in other indicators (besides CCR5 occupancy and viremia), so it's not obvious that leronlimab would help with the inflammation.
The actual paper lists the top ones. Chemokines CCL2, CCL8 bind directly to CCR5. CCL20 is upregulated by CCR5. A wide variety of interferons are upregulated by CCR5.
https://iiam.org/wp-content/uploads/2017/01/IIAM_ResearcherArticle11.pdf
In general you would be correct that immunomodulator drugs are best only for extreme cases. That's because they also downregulate the ability of the immune system to directly fight the virus. However leronlimab's secret weapon is that it increases the immune system's ability to kill the virus.
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