"My point is my concern that just binding to pipe/envelope-proteins on *unactivated* virus my not be sufficient to halt incubation on progress into full blown infections? "
Step 1 is to derive neutralizing antibodies against what they put in the mouse (pseudovirus). Step 2 is testing them for efficacy against live virus in the animals. They have made this point clear before, multiple times. That is part of what will take time to get into clinic. Otherwise they could select best Abs probably in a flash and be done with it.
"Interesting, virus avoid immune system for prolonged time,...so how to break this *tolerance* and activate *adaptive* response? len is talking about passive immunization? Really?"
Providing antibodies to someone is the definition of passive immunization. Because their body hasn't made them itself. That is what passive immunity means.
"The greatest reduction in mortality (minus 22.5 percent) across all study groups occurred with REGN-EB3 treatment in patients who were treated later in the course of their disease, when risk of dying from Ebola is greatest." REGN-EB3 demonstrate to be effective as TREATMENT, not only prophylactic agent."
I think you are misinterpreting that comment, it is referring to effect size of relative benefit vs. other treatments. Your interpretation directly contradicts this from NEJM as well as statements from Regeneron to this effect that those caught and treated earlier had even fewer deaths and the better mortality results vs. patients caught later (on same REGN treatment).
"In addition to differential effects of the four trial agents with respect to mortality, the results showed the importance of early diagnosis and treatment. We observed an 11% increase in the odds of death for each day that symptoms persisted before enrollment. These data highlight the need for community awareness that earlier diagnosis and treatment are associated with increased survival. Similarly, there was an effect of baseline viral load with respect to death at 28 days with each trial drug: mortality among patients who had a nucleoprotein Ct value of 22 or less at screening (i.e., high viral load) was 4 times as high as mortality among patients with a nucleoprotein Ct value of greater than 22 (i.e., low viral load)."
"REGN-EB3 demonstrate to be effective as TREATMENT, not only prophylactic agent. Was this due to TRUE knowledge of the Ebola biology and *INTERVENTION POINTS* Abs design, or just due to SUPERIOR mouse model and LUCK! I think former one. Unfortunately."
I guarantee you, no antibodies are getting inside cells, no matter whether they are designed against Ebola virus, Wuhan virus, interleukin receptors, or anything else.
Regn has made it clear this is being developed as both a potential prophylaxis (for at-risk healthcare providers) AND as a treatment for infected patients |
