CTMedic was kind enough to send me a link to a study.
Increased mTOR signaling, impaired autophagic flux and cell-to-cell viral transmission are hallmarks of SARS-CoV-2 infection.
Our findings reveal that SARS-CoV-2 infection in Vero E6 cells and severe COVID-19 patients occur in conditions of increased mTOR activity and impaired autophagic flux that could prevent the viral release and promote cell-to-cell viral transmission.
My earlier proposed anti-viral activity of leronlimab -
CCR5 blockade of CCL5 disrupts the PI3K/AKT/mTOR/4E-BP1 pathway dysregulating elF4E. With elF4E disrupted the COVID-19 virus 5' -end cap would be unable to separate it's mRNA and duplicate.
Elevated mTOR would increase viral reproduction. If I remember correctly CA2+ is also necessary to the viral reproduction process and leronlimab downregulates that. Which is why I think a properly done mild/moderate trial could beat molnupiravir and REGN-COV2.