A couple of days ago I had a look at Iwasaki's paper on the features of Long Covid by an immune profiling because it is that paper that they found their rationale to go after the role of pathogens in LC and ME/CFS, especially herpes viruses.
Individuals with long COVID show marked biological changes in cortisol and immune factors relative to convalescent populations.
www.nature.com
It seems it doesn't have its own page yet on s4ME.
She found reactivated EBV and – fanfare – VZV or HHV-3.
They say they found proof of the reactivation of these two viruses neither via anti-bodies, nor through PCR but by some molecule you find in reactivation but that's probably expensive and technology intensive to pin down. I don't understand these details, unfortunately.
I of course thought that this was very interesting because aciclovir has very good activity against VZV.
all antivirals have metabolic effects that have nothing to do with inhibiting viral DNA or RNA synthesis directly. Many antiviral drugs inhibit the key metabolic enzyme SAdenosylhomocysteine Hydrolase (SAHH). Inhibition of SAHH causes an increase in intracellular SAH levels. SAH is a potent inhibitor of DNA, RNA, protein, and small molecule methylation. This affects both viral and host cell epigenetics, gene expression, mRNA translation, and protein stability.
explaining some detail of the pharmacology of antivirals. I checked for aciclovir. Aciclovir does not do that. – I wondered whether the discussion above were about such ideas of the workings of antivirals in general.
I have no knowledge of antivirals exept some of aciclovir.
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