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SIGA Technologies, Inc. Message Board

  • amlnlover100 amlnlover100 Aug 2, 2013 9:40 AM Flag

    ST-610 Looks Good

    I’d like to anticipate a criticism of ST-610 from the abstract. SIGA speaks of “Sequence analysis of drug-resistant virus isolates has identified a single point mutation…”. Now, some might say “Oh, great, resistant strains pop up!”. But, for such a disease, it’s not important, and I’ll tell you why. Now, I’m not a certified virologist (but, I have had the flu many times, and some unknown rash once “down there”).

    Anyway, dengue normally exists in a transmission cycle between mosquitoes and animals like pigs, birds, and small water mammals. These things are called the “host reservoir”. Now once in a while a mosquito bites a person and gives him the disease from one of these animals, which ST-610 will then cure. The only possible “resistance” issue would be a person taking ST-610 developed a resistant strain during therapy, and a mosquito bit him, and then bit another person, and delivered the ST-610 resistant strain to them…. Unlikely.

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    • Or if the mosquito picked up resistant strain and then bit a pig.. This is the problem in influenza with neuraminidase inhibitors. The important issue is whether the mutation confers greater survivability than the wild type outside of the human host and without the presence of the antiviral. If not, then the mutated version dies outside of the treated host. The other important thing to keep in mind is that dengue isn't transmitted directly through droplets or direct contact. It is a blood-borne disease.

      • 1 Reply to musherga
      • "Or if the mosquito picked up resistant strain and then bit a pig."

        Actually, that is not a problem. You see, the mutation that provides resistance is a spontaneously arising event. That is, the mutation occurs in an animal under ST-610 therapy at the exact same frequency that it occurs in the wild. It is a “recessive” (so to speak) mutant, constantly occurring, but not prevailing in the wild. It therefore, by definition, it must contribute a competitively disadvantageous phenotype to the wildtype strain. And, as it is a “point” mutation, it is easily “repairable” in natural infections (a single codon "swaps" back to wildtype as easily as it occurred). So, I still have not heard of any mechanism to establish an epidemiologically significant ST-610 resistant strain.

        Well, anyway, that’s what the host at the Holiday Inn I stayed in last night told me. Before he gave me a cookie…

 
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