(I’ve repeatedly had to update in the direction of it being plausible, and I currently think it’s more-likely-than-not to be a factor that will complicate vaccine development.)
Other coronaviruses, ex: FIP, have had vaccines that presented with this problem (imperfect antibodies against the vaccine resulted in increased severity of illness compared to baseline).
An in-vitro experiment suggesting that nCOV could use imperfect antibodies as a viable “anchor” for infecting white blood cells. Was tested using previous SARS-1 vaccines.
Interpretation: Assuming it’s the same case among SARS subtypes, antibodies against the spike-protein are a bad idea, but antibodies against other components of the virus (which don’t evolve as fast as the S-protein) seemed to work. The one N-protein vaccine didn’t have this bad effect.
Interpretation: in-vitro isn’t nearly as conclusive as in-vivo, though...
A preprint suggesting that ADE may already be part of why we have such wide variance in the severity of symptoms. Severe cases may be severe in part because of this exacerbating response to non-neutralizing antibodies.
Interpretation: Geez, this actually seems to match-up with the disease pattern well. The elderly have worse immune responses and tend to be more prone to poorly-constructed antibodies (resulting in things like ex: autoimmune responses), and the high-severity disease tends to happen late (around when the antibody-based adaptive immune response kicks in). I need to double-check, but if kids have better innate immune responses, it fits fantastically. The white blood cell deficiencies which the paper mentions occur in the severe cases feels fairly conclusive to me.
This proposes that China may have had a far-worse death rate in part because of exposure to previous cases of SARS-1.
Interpretation: At least a few points towards the hypothesis, but my prior was that a zoonotic disease straight-off-the-literal-bat would be more severe anyway.
T-cell exhaustion may have some bearing on this question, as either evidence or counter-evidence depending on whether the infected/dying immune cells are specifically Fc-bearing or not.
(ADE is likely to specifically affect Fc receptor bearing cells, which consist of: B lymphocytes, follicular dendritic cells, natural killer cells, macrophages, neutrophils, eosinophils, basophils, human platelets, and mast cells. I need to run throgh the preprint on symptom-variance and double-check the types of WBC affected.)
Future prediction: People who had the SARS-1 or MERS vaccine previously (esp. if vs. S-protein, which most include) will tend to get more severe cases with SARS-2.
The possibility of Antibody-Dependent Enhancement looks very real, to me.
(I’ve repeatedly had to update in the direction of it being plausible, and I currently think it’s more-likely-than-not to be a factor that will complicate vaccine development.)
Other coronaviruses, ex: FIP, have had vaccines that presented with this problem (imperfect antibodies against the vaccine resulted in increased severity of illness compared to baseline).
An in-vitro experiment suggesting that nCOV could use imperfect antibodies as a viable “anchor” for infecting white blood cells. Was tested using previous SARS-1 vaccines.
Interpretation: Assuming it’s the same case among SARS subtypes, antibodies against the spike-protein are a bad idea, but antibodies against other components of the virus (which don’t evolve as fast as the S-protein) seemed to work. The one N-protein vaccine didn’t have this bad effect.
Interpretation: in-vitro isn’t nearly as conclusive as in-vivo, though...
A preprint suggesting that ADE may already be part of why we have such wide variance in the severity of symptoms. Severe cases may be severe in part because of this exacerbating response to non-neutralizing antibodies.
Interpretation: Geez, this actually seems to match-up with the disease pattern well. The elderly have worse immune responses and tend to be more prone to poorly-constructed antibodies (resulting in things like ex: autoimmune responses), and the high-severity disease tends to happen late (around when the antibody-based adaptive immune response kicks in). I need to double-check, but if kids have better innate immune responses, it fits fantastically. The white blood cell deficiencies which the paper mentions occur in the severe cases feels fairly conclusive to me.
This proposes that China may have had a far-worse death rate in part because of exposure to previous cases of SARS-1.
Interpretation: At least a few points towards the hypothesis, but my prior was that a zoonotic disease straight-off-the-literal-bat would be more severe anyway.
T-cell exhaustion may have some bearing on this question, as either evidence or counter-evidence depending on whether the infected/dying immune cells are specifically Fc-bearing or not.
(ADE is likely to specifically affect Fc receptor bearing cells, which consist of: B lymphocytes, follicular dendritic cells, natural killer cells, macrophages, neutrophils, eosinophils, basophils, human platelets, and mast cells. I need to run throgh the preprint on symptom-variance and double-check the types of WBC affected.)
Future prediction: People who had the SARS-1 or MERS vaccine previously (esp. if vs. S-protein, which most include) will tend to get more severe cases with SARS-2.
I know FIP as feline infectious peritonitis
Is that what you are referring to?