Havasu, I'm late to respond. However, you are c
Post# of 154704
(Total Views: 574)
Posted On: 01/27/2022 6:49:25 AM
Havasu,
I'm late to respond. However, you are correct. Leronlimab effectively only treats the cytokine storm (immune cell trafficking and dysregulation. Likely NETosis and coagulopathy as well, but appropriately grouped together for general discussion).
Delta and previous variants were dependent on TMPRSS2 as the cell fusion and entry mechanism while Omicron utilizes both TMPRSS2 and endosomal entry. Omicron is thus able to target more cell types, including upper airway cells which were mostly spared by Delta, but is still able to infect lower airway/alveolar cells albeit with lower efficiency.
As a generalization, patients don't become critically ill from viral respiratory diseases without immune dysfunction. Very few end up in the ICU or die from "typical" cold viruses (rhinovirus or any of the endemic coronaviruses).
Omicron has displaced delta, yet thousands are still dying daily, 3143 in US yesterday. Previous infection, vaccination, and lower omicron virulence (estimated 30-50% reduction) result in lower mortality rates, but the overall numbers are still unacceptable.
Covid will be with us IMO for generations, likely at high endemic level. Influenza kills ~35K on average in the US. Leronlimab resolves immune dysfunction irrespective of the variant of Covid, with a similar efficacy expected for immune dysfunction from other pathogens.
A bit down the road, but there is reason to expect that Leronlimab will treat critical disease from influenza and sepsis from a host of pathogens.
Time will tell.
I'm late to respond. However, you are correct. Leronlimab effectively only treats the cytokine storm (immune cell trafficking and dysregulation. Likely NETosis and coagulopathy as well, but appropriately grouped together for general discussion).
Quote:
My suspicion is that in Cytodyn clinical trials leronlimab will be limited to treatment of patients with cytokine storm.
Delta and previous variants were dependent on TMPRSS2 as the cell fusion and entry mechanism while Omicron utilizes both TMPRSS2 and endosomal entry. Omicron is thus able to target more cell types, including upper airway cells which were mostly spared by Delta, but is still able to infect lower airway/alveolar cells albeit with lower efficiency.
As a generalization, patients don't become critically ill from viral respiratory diseases without immune dysfunction. Very few end up in the ICU or die from "typical" cold viruses (rhinovirus or any of the endemic coronaviruses).
Omicron has displaced delta, yet thousands are still dying daily, 3143 in US yesterday. Previous infection, vaccination, and lower omicron virulence (estimated 30-50% reduction) result in lower mortality rates, but the overall numbers are still unacceptable.
Covid will be with us IMO for generations, likely at high endemic level. Influenza kills ~35K on average in the US. Leronlimab resolves immune dysfunction irrespective of the variant of Covid, with a similar efficacy expected for immune dysfunction from other pathogens.
A bit down the road, but there is reason to expect that Leronlimab will treat critical disease from influenza and sepsis from a host of pathogens.
Time will tell.
(8)
(0)