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Posted On: 02/05/2021 1:03:49 AM
Post# of 155794
Thanks for this.
“In natural CCR5 delta 32 double allele gene absence other receptors will take over a large part of the load. Just gene editing out CCR5 would leave you in the same position as gene edited mice. You would be very susceptible to infections since the immune system is completely impaired”
I recalled that Leronlimab occupies CCR5 receptors without limiting normal immune function. But I certainly did not realize that according to your example above, that natural CCR5 absence could be mitigated (?) by other chemokine receptors. This in opposition to gene edited CCR5 absence, as in mice or the Chinese twins, leaving the immune system vulnerable.
I wonder what deferential considerations are being given to the twins for life.
“In natural CCR5 delta 32 double allele gene absence other receptors will take over a large part of the load. Just gene editing out CCR5 would leave you in the same position as gene edited mice. You would be very susceptible to infections since the immune system is completely impaired”
I recalled that Leronlimab occupies CCR5 receptors without limiting normal immune function. But I certainly did not realize that according to your example above, that natural CCR5 absence could be mitigated (?) by other chemokine receptors. This in opposition to gene edited CCR5 absence, as in mice or the Chinese twins, leaving the immune system vulnerable.
I wonder what deferential considerations are being given to the twins for life.
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