So as per Otto Yang, the immune systems of these long haulers was non-existent. Hardly in operation, dead for all intents an purposes.
That would mean no Interferon Alpha, or Gamma to start with.
Then LL is given. LL binds to what ever CCR5 is available and after a few weeks, many more CCR5 are found on the cell surfaces.
Interferon Gamma, Alpha would get expressed by the cells, if they awake from the dead. When LL binds to CCR5, the cells begin to awaken some how and then begin to express interferon alpha and gamma.
With the accumulating beneficial effects of giving LL week after week for the length of the trial ~8 weeks maybe? the end result was evidence that LL helped the patient in long haulers and increased CCR5 expression on CD4 cell surfaces. We are assuming increased Interferon Gamma and Interferon Alpha and Interleukin 10 etc..., but can't say for sure, but most likely that too happened.
So what you are suggesting is that with the 1st dose of LL, the binding of LL to CCR5 was enough to get the ball rolling. LL binds to CCR5 and then the cell awakens from its trance, (likely CCL5 RANTES induced). That would mean CCL5 was displaced by LL by the way. With CCL5 out of the way and LL bound to CCR5, the cell wakes up and begins to go to work. It starts producing the cytokines of interferon we are discussing.
The increased cytokines of interferon alpha and gamma induce with in the CD4 cell itsef an internal response to produce more CCR5 receptors on its surface.
With the next injection of LL, the newly created CCR5 receptors are bound to by LL and the cell continues to work to fight the spike proteins that long haulers is. Even more interferon is produced and even more CCR5 are manufactured internally to the CD4 cell and then expressed externally on their surfaces.
By the binding of LL to CCR5, more of the interferons are free floating because LL got rid of the CCL5 RANTES that tricked the cell into believing that nothing was wrong and not to produce the inflammatory cytokines of interferon gamma,etc. When LL took over, the interferons were produced and that induced a response within the CD4 cell to express more CCR5.
That would mean no Interferon Alpha, or Gamma to start with.
Then LL is given. LL binds to what ever CCR5 is available and after a few weeks, many more CCR5 are found on the cell surfaces.
Interferon Gamma, Alpha would get expressed by the cells, if they awake from the dead. When LL binds to CCR5, the cells begin to awaken some how and then begin to express interferon alpha and gamma.
With the accumulating beneficial effects of giving LL week after week for the length of the trial ~8 weeks maybe? the end result was evidence that LL helped the patient in long haulers and increased CCR5 expression on CD4 cell surfaces. We are assuming increased Interferon Gamma and Interferon Alpha and Interleukin 10 etc..., but can't say for sure, but most likely that too happened.
So what you are suggesting is that with the 1st dose of LL, the binding of LL to CCR5 was enough to get the ball rolling. LL binds to CCR5 and then the cell awakens from its trance, (likely CCL5 RANTES induced). That would mean CCL5 was displaced by LL by the way. With CCL5 out of the way and LL bound to CCR5, the cell wakes up and begins to go to work. It starts producing the cytokines of interferon we are discussing.
The increased cytokines of interferon alpha and gamma induce with in the CD4 cell itsef an internal response to produce more CCR5 receptors on its surface.
With the next injection of LL, the newly created CCR5 receptors are bound to by LL and the cell continues to work to fight the spike proteins that long haulers is. Even more interferon is produced and even more CCR5 are manufactured internally to the CD4 cell and then expressed externally on their surfaces.
By the binding of LL to CCR5, more of the interferons are free floating because LL got rid of the CCL5 RANTES that tricked the cell into believing that nothing was wrong and not to produce the inflammatory cytokines of interferon gamma,etc. When LL took over, the interferons were produced and that induced a response within the CD4 cell to express more CCR5.
