3 ms·

Was just hoping to point out for those who aren't as close to this space that the fact that non-neutralizing antibodies can bind is neither a positive nor negat

Was just hoping to point out for those who aren't as close to this space that the fact that non-neutralizing antibodies can bind is neither a positive nor negative signal. Also, what I wrote is not speculation: The potential danger of suboptimal antibody responses in COVID-19 (https://www.nature.com/articles/s41577-020-0321-6 https://www.nature.com/articles/s41577-020-0321-6) (Overview) COVID-19-neutralizing antibodies predict disease severity and survival (https://www.sciencedirect.com/science/article/pii/S0092867420316858 https://www.sciencedirect.com/science/article/pii/S009286742...)

timr 6y ago
Neither of these papers supports the claim you made. The first one explicitly says that antibody-dependent enhancement has not been observed for this virus: > There is no evidence that ADE facilitates the spread of SARS-CoV in infected hosts. In fact, infection of macrophages through ADE does not result in productive viral replication and shedding "suboptimal antibody responses" are indeed...suboptimal...but the paper here is not showing that. As the OP noted, the concerning result is limited to a few examples of monoclonal antibodies. The human immune response is much more complicated.
- chemeng 6y ago
  You edited your comment after I had responded, so hopefully I can address those concerns. I'm not sure the "claim" you think I am making. As for increased infectivity, that is at the core of what is understood to occur in ADE. And in general, cases where the Fc mediated response is utilized to gain entry to immune cells. I believe Dengue is the typical example spoken to, but this pattern has been observed in Zika, HIV, RSV off the top of my head. Lots of editing! Also, did not state that ADE occurs for SARS-CoV2. The fact that studies indicate it does not replicate or shed after phagocytosis is a positive signal.
  - timr 6y ago
    > I'm not sure the "claim" you think I am making. As for increased infectivity, that is at the core of what is understood to occur in ADE. >> In many cases, binding antibodies increase cell infectivity. ^ This is what you wrote. It is unsupported. ADE is rare, and it has not been observed with this virus.

timr 6y ago

Neither of these papers supports the claim you made. The first one explicitly says that antibody-dependent enhancement has not been observed for this virus: > There is no evidence that ADE facilitates the spread of SARS-CoV in infected hosts. In fact, infection of macrophages through ADE does not result in productive viral replication and shedding "suboptimal antibody responses" are indeed...suboptimal...but the paper here is not showing that. As the OP noted, the concerning result is limited to a few examples of monoclonal antibodies. The human immune response is much more complicated.

chemeng 6y ago
You edited your comment after I had responded, so hopefully I can address those concerns. I'm not sure the "claim" you think I am making. As for increased infectivity, that is at the core of what is understood to occur in ADE. And in general, cases where the Fc mediated response is utilized to gain entry to immune cells. I believe Dengue is the typical example spoken to, but this pattern has been observed in Zika, HIV, RSV off the top of my head. Lots of editing! Also, did not state that ADE occurs for SARS-CoV2. The fact that studies indicate it does not replicate or shed after phagocytosis is a positive signal.
- timr 6y ago
  > I'm not sure the "claim" you think I am making. As for increased infectivity, that is at the core of what is understood to occur in ADE. >> In many cases, binding antibodies increase cell infectivity. ^ This is what you wrote. It is unsupported. ADE is rare, and it has not been observed with this virus.