Question by Raqib Zaman:
So how does the body deal with lipid-enveloped viruses? Can they be targeted by going into mild-ketosis (fasting)??
Answer by Steven Fowkes:
The concept of biological terrain dates back about two centuries. About one century ago, Dr. Revici studied this in animal disease models. What he discovered is that microbes have a preference for certain kinds of terrain in their hosts, and if you give them that environment, they become more virulent. When anthrax was passed through rodents who were fed a cholesterol-rich diet, the anthrax became lethal. But when the anthrax was then passed through rodents on a high fatty acid diet, the anthrax became non-lethal.
This shows that microbes adapt to their environment just like higher life forms do. Then there is host resistance, which I talked about. You can think about this as immune-system function, but it goes far beyond that. I’ve been studying the effect of BHT (butylated hydroxytoluene) as an antiviral agent since 1975, and it shows strong antiviral properties even in people who have hypometabolism and other aspects of immune dysfunction. The original hypothesis, by the original research team, was that BHT disrupted the lipid envelope and dislodged a binding protein needed for infectivity. But this turned out to be an artifact of their study. So BHT works by some kind of non-specific mechanism that is shared by other substances. What they all have in common is a concerted metabolic effect, which is another way of saying that they produce an antiviral terrain. There are a few other posts which go into this on Quora. Selenium, for example, is substantially antiviral element against roughly half of all viruses. This cannot be explained by any kind of toxic or pharmacological (receptor-driven) mechanism.
That’s not to say that some things might have a direct lipid-destabilizing effect. But this has not been observed with BHT, vitamin A, B12, reduced-sulfur and nitroxide spin-label compounds (e.g., glutathione and BPN, repectively).
The selenium connection with hemorrhagic viruses (e.g., ebola) is at least partially explained by the presence of seleno-aminoacid codons in the viral DNA. But it is hypothesized (so far) that this is the mechanism of the hemorrhagic effects only.