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The point is you proposed, to my knowledge, a new indication for leronlimab without an explanation as to what the mechanism of action might be for treating severe cases of influenza and how you would propose that we go about determining this.

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If you want to know the extensive MOA of leronlimab go read hundreds of medical papers, I have. Do you think I'm pulling this out of thin air? The very, very basic MOA is that leronlimab blocks the CCR5 receptor, which stops chemokines from attaching and directing the macrophages to sites of infection. We could go into interferon activity, macrophage production cycles and oh so much more, but that's all that's needed. The macrophages (T-cells specifically in this case) can overwhelm the organ in question causing inflammation and excessive cell death potentially leading to the death of the patient.

How would you determine if the patient would benefit from treatment? Does the patient have Influenza? If yes, is the patient at risk of dying due to an over-responsive immune system and inflammation? If yes, is the patient not a CCR5 delta 32 deletion carrier? If not, a CCR5 occupancy test can set the level of dosage to treat the patient.

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So far, leronlimab seems to not effect normal immune functions

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It limits normal immune response. If there was no limitation then it would not work in cancer. You may say: But wouldn't that increase the danger to the patient by limiting immune response to influenza? With an over-response by the immune system, that's what's going to kill them.

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however, a population of 800 is still small and I have no idea if any of these patients experienced an influenza infection while taking leronlimab.

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If I remember correctly several of the pre-10 week patient's viral spikes were caused by just that.

PS. They didn't die.