The mix of correct and incorrect 'facts' on the back and forth postings here is just going to confuse people. See bottom of this post for what is the truly important difference between vaccines and EbolaCide2 (IMH speculation).
Here is what we know and don't know - from memory, so hopefully I can get through without a mistake.
1. CASE 1: For EbolaCide2 given to patients already sick with Ebola.
a. EbolaCide2 would eventually destroy some or all of the virus (assuming efficacy).
b. The immune system would produce a broad spectrum of antibodies to multiple sites of the fully virulent form of the virus.
c. Patients would have immunity to that version of Ebola.
d. High probability that patients would have at least partial immunity to mutated versions of Ebola.
2. CASE 2: For EbolaCide2 given prophylactically to e.g. healthcare workers
a. EbolaCide2 would circulate in bloodstream for maybe a month with initial high but diminishing protection should they be exposed to Ebola.
b. If not exposed to Ebola, workers would NOT develop antibodies to Ebola and eventually not be protected unless given additional EbolaCide2 doses.
c. If exposed to Ebola, workers would have some EbolaCide2 protection, develop immunity to that version of Ebola and likely at least partial immunity to mutated versions (same as above Case 1).
3. CASE 3: For some other company's vaccine given to healthcare workers
- Vaccine options would include: a weakened (attenuated) live virus; or dead (inactivated) virus; or parts of virus (proteins, genetic material, etc. often made in laboratories). For Ebola, the only viable option is the latter (man-made parts of virus).
a. If the vaccine is made from portions of the virus that can mutate without the virus losing viability, it will not be effective against mutated versions of the virus - or may not be effective at all (e.g. if it targets the chaff like the soluble glycoproteins sloughed off by Ebola).
b. If vaccine is made from highly conserved portions of the virus that are necessary for infection to remain viable (and if those portions are accessible to antibodies in the bloodstream), the vaccine will provide protection from not only the version modeled, but also at least partially to mutated versions of the virus.
Case 3b is analogous for vaccines and EbolaCide2. If either option is to work, the right portions of the virus need to be targeted and either accessible or made accessible to either antibodies or 'Cides. Neither option - 'Cides or vaccines is truly unique for protection against mutated versions of viruses if they both target conserved portions of the viruses necessary for infection.
However, 'Cides do provide another potential advantage over vaccines. What I am talking about are the glycan caps that mask attachment to the NPC1 portion of Ebola.
Vaccines could mimic the NPC1 portion of Ebola to generate antibodies to it. But unless those caps are removed from the virus somehow, the antibodies may not be able to attach and summon an immune response in circulation (although maybe in a more limited way through attachment when the caps are removed in the endosome before release of the viral genetic material into the cytoplasm of the cell).
EbolaCide2 could mimic the receptors to NPC1 to attract attachment by Ebola. But unless the caps are first removed, Ebola will also not chemically attach to EbolaCide2 in circulation (although maybe in limited quantities in the endosome).
This is where EbolaCide2, in theory, may have its true advantage over vaccines. Additional ligands can be added to EbolaCide2 to remove the caps prior to NPC1 ligand attachment. As Dr. Seymour pointed out, there is literature now elucidating the sequelae of Ebola infection. Cathepsin has a known role in cap removal prior to NPC1 attachment. It is likely (IMHO) that Cathepsin and/or other ligands were added to EbolaCide2 to remove the glycan caps and allow subsequent attachment to the NPC1 ligands. If so, there is more promise with EbolaCide2 than with the vaccine alternatives.
