Cross-posting from a response I wrote on the Longecity forum:
Rider’s PLOS1 paper said that it worked for 15 viruses but didn’t list Epstein Barr Virus as one it could cure. That got my interest because EBV is a very common virus but has an apoptosis blocking mechanism that prevents assembly of the DISC protein necessary to trigger RIP to trigger necroptosis that DRACO uses. This makes me think that it won’t be effective in 80% of the population who has EBV. Since EBV is very common I was wondering if he ever tested it on EBV and didn’t report the result which would seem to be failure.
Necroptosis is a form of programmed cell death that results in necrosis. In necrosis, a cell effectively lyses and releases its interior contents to the surrounding environment. Because of that, necrosis activates the immune system, causing inflammation and other downstream effects. As I explain in my thread here:
We don't want necrosis, and DRACO doesn't use necrosis. Therefore, the necroptosis pathways don't matter. Necroptosis is also known as "Caspase Independent Cell Death" (CICD). DRACO actually relies on Caspase dependent pathways.
Dr Rider reported success against 15 viruses. As a scientist and researcher, finding a virus that didn't respond as expected to DRACO would have been an important result, and would not have diminished his work in any way. There's no indication in his paper or elsewhere that he tested for it and didn't report a negative. In fact, in his 2015 crowdfunding pitch, he explicitly mentions wanting to test against Herpesviruses, including EBV:
https://www.indiegogo.com/projects/dracos-may-be-effective-against-all-viruses#/
There would be no reason for him to propose that if he had already done the work.
"DRACO" is actually a family of compounds. One formulation, PKR+Apaf, works on the apoptosis side by activating Procaspase 9 (which then activates Caspase 9 --> Caspase 3). It turns out that EBV also activates Caspase 9, but without triggering apoptosis. On that basis (rather than on the TRIF / RIP side where EBV also interferes), it is possible that PKR+Apaf may not be effective against EBV. We won't know for sure until we test it (although in the Herpesvirus family, CMV is currently a higher priority for us than EBV, due to its probable effects on aging).
Even though EBV interferes with the Caspase 9 pathway in some way, that alone isn't reason enough to say for sure that PKR+Apaf won't work. Let's not forget the PKR half of the protein. The process of DRACO binding with dsRNA by itself also interferes with viral replication, even if apoptosis isn't triggered. If replication is slowed down enough, it's possible that the compounds interfering with Caspase 9 will fade faster than DRACO does. Rider showed that a single dose of DRACO lasts for at least 8 days in some cells, and of course in a therapeutic situation, multiple doses are possible. Again, we won't know for sure until we test. Which we're going to do.
In addition, if EBV does manage to evade PKR+Apaf, other formulations are possible. Rider tested PKR+FADD, for example, which works by activating Procaspase 8 --> Caspase 3, entirely bypassing Caspase 9. Using PKR+Caspase 3, which is the immediate precursor to the protein cleavage that results in cell death, may also be possible. Using RNase L instead of PKR is another possibility (which Rider also tested). It may produce different results because RNase L acts to degrade the dsRNA, hopefully crippling the virus in the process, while the effector domain also working to cause apoptosis.