Enteroviruses - revisited

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10
What I hope to be able to do is increase my interferon suppository dose level to just below the threshold where I can feel increased depression kicks in, and then keep it at that dose level for some time, to see if my ME/CFS symptoms slowly improve. If my ME/CFS does improve, then I will consider taking low dose interferon indefinitely, as we know from Dr Chia's interferon treatment studies that all his ME/CFS patients who were in remission relapsed once they stopped the treatment.

@Hip Given two things: A) my own experience of possibly getting CFS from a course of Ribavirin and Interferon alpha and B) Prof Ron Davis' mentioning the interferon alpha is implicated negatively in the path to ME/CFS, did this experiment go poorly?

Sorry to the late unearthing of this old post. I'm resuming my treatment quest and have had PR down as my resource for potential treatments, with a focus on targeting coxsackie, EBV, CMV, etc. So I'm actually here to try and find out what the latest info is about selecting treatments, but this interferon alpha thing is a biggy to me personally, so any insights you could share would be appreciated.
 

Hip

Senior Member
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18,148
So I'm actually here to try and find out what the latest info is about selecting treatments

I don't think there is much new, unfortunately. For enteroviruses, Dr Chia uses oxymatrine, tenofovir and Epivir as he has always done. For herpesviruses, Valcyte seems to get the most improvements, but I read Stanford stopped using Valcyte a few years ago due to the low success rate.
 
Messages
10
I don't think there is much new, unfortunately. For enteroviruses, Dr Chia uses oxymatrine, tenofovir and Epivir as he has always done. For herpesviruses, Valcyte seems to get the most improvements, but I read Stanford stopped using Valcyte a few years ago due to the low success rate.
Thanks for the info.
 

mrmichaelfreedmen

Senior Member
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173
Location
Australia
Large doses can be dangerous. The study I read said anything over 600mg per day is not recommended. From memory it can cause shortness of breath by interference of oxygen metabolism - Along those lines, report back with link.

I get shortness of breath with high (1000mg) doses of NAC. I take 500mg twice a day and find it fine at this dose. I have read different opinions from health professionals who caution high NAC doses.
 

Hip

Senior Member
Messages
18,148
have you had your nagalase levels checked? High levels would indicate a reason why Oxymatrine did not work.

I never got checked for nagalase.

May I ask, where did you see that high nagalase might thwart oxymatrine? High nagalase is thought to thwart GcMAF, but I've not seen a connection to oxymatrine before.
 

mrmichaelfreedmen

Senior Member
Messages
173
Location
Australia
I never got checked for nagalase.

May I ask, where did you see that high nagalase might thwart oxymatrine? High nagalase is thought to thwart GcMAF, but I've not seen a connection to oxymatrine before.

High Nagalase prevents the macrophages from activating, so the immune cascade of events do not occur (or at least severely limit).

The chart I saw displayed the macrophages right at the top of this cascade, and the Th1 etc response was right at the bottom.

They referred to the macrophages activating like turning the key in your vehicle, no key turn, no activation.

I suspect that this is why Oxymatrine only works in 50% of patients Dr Chia treats.

Will try and find where I read this explanation.
 

Husband of

Senior Member
Messages
326
Isn't baricitinib just an anti-inflammatory? I don't think this would have any antiviral effects.
"In our previous correspondence we suggest that the combined anti-inflammatory and AI-predicted antiviral activities [9, 10] of the rheumatoid arthritis drug baricitinib would be potentially a effective treatment for those infected with SARS-CoV-2."

https://link.springer.com/article/10.1007/s00415-020-09866-5

From one of the sources:
The drug targets are members of the numb-associated kinase (NAK) family—including AAK1 and GAK—the inhibition of which has been shown to reduce viral infection in vitro.
5,
6Baricitinib was identified as a NAK inhibitor, with a particularly high affinity for AAK1, a pivotal regulator of clathrin-mediated endocytosis. We suggested that this drug could be of use in countering SARS-CoV-2 infections, subject to appropriate clinical testing.
Link: https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(20)30132-8/fulltext

Baricitinib they say is good at getting across the blood brain barrier and into the csf. Meaning it could help those with COVID in the brain or csf.
 
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