FIP Treatment

Well, I wish I knew.

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The baffling thing is that the treatment works in only a few minutes, even in critical cases. This had me stumped for almost a year until I thought that if it happened every time, there must be an explanation: if there was not time for the supplements to reach the stomach, then they must be absorbed before the stomach. After reading up on transbuccal absorption I was convinced that this must be the explanation that I was looking for. In essence, it seems that some molecules are able to squeeze through the buccal mucosa and enter the bloodstream almost instantly. This doesn’t seem to work with complex or hydrophobic molecules, but apparently it is the mechanism behind transdermal gels, sublingual lozenges and nicotine patches.

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One part of the puzzle seems to be solved. Now I need to find out how an inexpensive supplement can kill a virus with a higher mortality rate than FIP or FeLV. Well, I don’t think it is actually killing the virus, but I have a few theories.

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Initially, I thought that the treatment was activating the mechanisms of hematopoiesis or boosting thymic activity. This would be great because it would mean that other infections could also be treated this way.

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My second theory was that it somehow triggers a chemical cascade that is key in the neutralisation of this particular virus. I still had the feeling that these processes would take significantly more than five minutes.

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It’s also possible that one or more components of the treatment is binding to the viral capsid —or to the plasma membrane perhaps— so that the virus is unable to infect the cells or evade the complement-activated lysis mechanisms. Perhaps the antiviral effects are mediated by viral envelope disruption or an upregulation of reactive oxygen species. I would very much like to know if a substance can attach to the plasma membrane so that the virus is no longer attracted to the susceptible cell, or is unable to bind to the membrane receptors. This could perhaps be achieved by changing the electrical charge of the membrane, or its chemical structure.

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Then a vet told me that if the treatment was working so quickly, the cause must be a nutrient deficiency. This is not possible because neonates were getting high fever and diarrhoea about ten days after being in contact with my other cats, and they were of course still on kitten formula. 

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But this got me thinking about something else. Perhaps there was a nutrient deficiency, but it was the virus —or, indirectly, the immune system— that was causing it. So this is my fourth theory: it’s possible that if there is a viral overload some micronutrients are being depleted, either by the virus when it replicates in the cat’s cells, or by the lymphocytes that are using up these micronutrients as fuel for physiological processes. If the virus is replicating a millionfold, then immunocytes also need to work a million times harder and need a commensurable amount of fuel. If there is a nutrient depletion the whole immune system stalls and the virus is able to go on infecting other cells.