>>So far, looks like the people in the US, especially Anglo-Saxons (just the fact, no racial profiling), has some group immunity.<<
I don't know jack about immunology, although I struggle mightily because I have rheumatoid arthritis, which is a nasty autoimmune disease which causes my macrophages to attack the synovial lining of my joints.
As autoimmune diseases go, it's not the worst (that would probably be muscular dsytrophy or maybe multiple sclerosis or myasthenia gravis) nor the best (well, none of them are good but the one that causes dry eyes seems to be the least debilitating).
There is definitely a genetic component to rheumatoid arthritis and pretty much every autoimmune disease, as far as I know.
At any rate, whatever is killing SARS patients may well have an autoimmune component - the host turns on itself, thinking it is killing the disease.
I can't help wondering whether tumor necrosis factor has a role in this -- if so, there are drugs which preferentially suppress tumor necrosis factor, including Remicade, Enbrel. , and Humira. Very expensive.
I take methotrexate which suppresses purine synthesis, used to take Arava which suppresses pyrimadine synthesis.
I have no idea how these work but I don't think that anybody really understands it yet. They inhibit protein synthesis which inhibits cell formation, so that slows down the growth of macrophages, but you need macrophages otherwise you die of infections. Oh, well, it works. Side effects - liver damage, lung damage.
Steroids are even more scatter-shot than methotrexate - essentially they act as an anti-feedback mechanism on the immune system.
Something more narrow is needed. What part of the immune system is over-reacting to SARS? I posted earlier a hypothesis that it's something to do with IgG2 and CD32 receptors -- and that Asians and Caucasians have different ratios of CD32 H131 vs. CD32 R131 -- only 10% of Asians are homozygous for the CD32 R131 phenotype
>>H131 is the high-binding allele and R131 is low binding, while heterozygotes have intermediate function. Because IgG2 is a poor activator of the classical complement pathway, Fc RIIa-H131 [CobaltBlue - this is another way of expressing CD32a-H131] is essential for handling IgG2 immune complexes. The genotype distribution of FcRIIA in Caucasian and African American populations is 25% homozygous for H131, 50% heterozygous, and 25% homozygous for R131. Among Asians, the frequency of the R131 allele is much lower, and 10% of the population is homozygous for R131.<<
Cached on google:
216.239.53.100 |
