EBV seems like arguably the most successful virus in history: it infects 90% of one of the most viable species (lifespan X population) and persists for life.
A few questions if you don't mind:
1. Are you on Twitter?
2. I don't have access to paper 17. Did the reactivation occur in B cells or epithelial cells? Did they reveal the specific factors or signaling pathways for reactivation? It makes sense for EBV to reactivate when the immune system is stressed, but I want to learn more about the specific triggers.
3. To replicate cell lines, why can't you manufacture EBNA1 with mRNA technology and avoid the plasmid altogether?
4. You mention, "the rate of MS is about 15-fold lower in EBV-negative individuals compared to EBV-positive ones." What's the lower bound (roughly) for meaningfulness? For instance, would 5x be considered meaningful? 2x?
5. Why are anti-EBV antibodies mostly ineffective at preventing infection? Don't we have a clear understanding of EBV antigens?
Very interesting, thank you!
Thanks for the deep and detailed analysis.
EBV seems like arguably the most successful virus in history: it infects 90% of one of the most viable species (lifespan X population) and persists for life.
A few questions if you don't mind:
1. Are you on Twitter?
2. I don't have access to paper 17. Did the reactivation occur in B cells or epithelial cells? Did they reveal the specific factors or signaling pathways for reactivation? It makes sense for EBV to reactivate when the immune system is stressed, but I want to learn more about the specific triggers.
3. To replicate cell lines, why can't you manufacture EBNA1 with mRNA technology and avoid the plasmid altogether?
4. You mention, "the rate of MS is about 15-fold lower in EBV-negative individuals compared to EBV-positive ones." What's the lower bound (roughly) for meaningfulness? For instance, would 5x be considered meaningful? 2x?
5. Why are anti-EBV antibodies mostly ineffective at preventing infection? Don't we have a clear understanding of EBV antigens?