I have just read elsewhere in the forum about Belimumab for Systemic Lupus Erythematosus.
https://forums.phoenixrising.me/index.php?threads/benylsta-belimumab-anyone-try-it.41437/
If I understand correctly, the mechanism of action is that Belimumab causes B-cells to die off more quickly and thus reduces autoimmune activity.
Now I am thinking the following: If you are targeting EBV with antiviral treatment - as I have done for 9 months with considerable success - the theory is that you stop EBV replication during reactivation. If EBV reactivates/replicates less, there are fewer B-cells it can infect and so, slowly over many months and perhaps even years, EBV activity in the body is reduced and recovery from EBV-caused CFS can occur.
Now if you take a drug that makes infected B-cells die off more quickly and at the same time, you stop EBV replication so any new B-cells cannot be infected, EBV activity in the body should be reduced much more effectively and response should occur more quickly.
From the information I have, Belimumab is relatively low-risk (especially compared to Rituximab) and in Germany, it's much cheaper:
https://www.medizinfuchs.de/preisve...-glaxosmithkline-gmbh-co.-kg-pzn-8878038.html
This is of course all speculation, but just in theory, could it enhance treatment for the subset of patients who strongly suspect EBV is to blame for their CFS and who have responded to EBV-targeting antivirals?
I look forward to hear your thoughts
https://forums.phoenixrising.me/index.php?threads/benylsta-belimumab-anyone-try-it.41437/
If I understand correctly, the mechanism of action is that Belimumab causes B-cells to die off more quickly and thus reduces autoimmune activity.
Now I am thinking the following: If you are targeting EBV with antiviral treatment - as I have done for 9 months with considerable success - the theory is that you stop EBV replication during reactivation. If EBV reactivates/replicates less, there are fewer B-cells it can infect and so, slowly over many months and perhaps even years, EBV activity in the body is reduced and recovery from EBV-caused CFS can occur.
Now if you take a drug that makes infected B-cells die off more quickly and at the same time, you stop EBV replication so any new B-cells cannot be infected, EBV activity in the body should be reduced much more effectively and response should occur more quickly.
From the information I have, Belimumab is relatively low-risk (especially compared to Rituximab) and in Germany, it's much cheaper:
https://www.medizinfuchs.de/preisve...-glaxosmithkline-gmbh-co.-kg-pzn-8878038.html
This is of course all speculation, but just in theory, could it enhance treatment for the subset of patients who strongly suspect EBV is to blame for their CFS and who have responded to EBV-targeting antivirals?
I look forward to hear your thoughts