NY is the place in America we have the most data, and are most likely to notice less common effects.
It fits with all the autopsy and clinical data that coagulation issues are a major cause of morbidity in severe cases, and the fact that children with non-severe cases are having an anomalously high rate of skin lesions in fingers and toes characteristic of circulation problems.
What I was really wondering about was does the particular strain of the virus matter here. My understanding is there are several different strains and what is primarily in the USA is not what was primarily in China or Europe.
Now that might just be poor news reporting on the facts as I’m not seem anything about -A, -B, -C versions.
For the most part, all those labels are just labels for where on the tree of all sequences it falls. There is almost no evidence of widespread functional mutants. They’re useful for tracking the spread of the virus around the globe.
There is one mutation in the S protein at the root of the European strains that you could *imagine* having an effect on the function of the fusion protein but there is no particularly strong evidence that it’s doing much—a little equivocal difference in the measured PCR cycles required for detection from samples, but that could have to do with the fact that they happened at different times when people were getting tested at different disease stages or on different equipment. It is more common more recently relative to the other lineages in Europe and America, but that could very easily just be because it is the only lineage in Italy and once Italy exploded its shrapnel founded a lot of new transmission chains all over Europe and America. It could very easily just be a bottleneck effect having to do with breaking into a new area.
Much more interesting are a few small lineages that have actually lost whole accessory proteins involved in suppressing the innate immune response, but that’s a total of like 7 patients found to have them.
NY is the place in America we have the most data, and are most likely to notice less common effects.
It fits with all the autopsy and clinical data that coagulation issues are a major cause of morbidity in severe cases, and the fact that children with non-severe cases are having an anomalously high rate of skin lesions in fingers and toes characteristic of circulation problems.
What I was really wondering about was does the particular strain of the virus matter here. My understanding is there are several different strains and what is primarily in the USA is not what was primarily in China or Europe.
Now that might just be poor news reporting on the facts as I’m not seem anything about -A, -B, -C versions.
For the most part, all those labels are just labels for where on the tree of all sequences it falls. There is almost no evidence of widespread functional mutants. They’re useful for tracking the spread of the virus around the globe.
There is one mutation in the S protein at the root of the European strains that you could *imagine* having an effect on the function of the fusion protein but there is no particularly strong evidence that it’s doing much—a little equivocal difference in the measured PCR cycles required for detection from samples, but that could have to do with the fact that they happened at different times when people were getting tested at different disease stages or on different equipment. It is more common more recently relative to the other lineages in Europe and America, but that could very easily just be because it is the only lineage in Italy and once Italy exploded its shrapnel founded a lot of new transmission chains all over Europe and America. It could very easily just be a bottleneck effect having to do with breaking into a new area.
Much more interesting are a few small lineages that have actually lost whole accessory proteins involved in suppressing the innate immune response, but that’s a total of like 7 patients found to have them.