Any extracts used in the following article are for non commercial research and educational purposes only and may be subject to copyright from their respective owners.
1) IS THE SPIKE PROTEIN DELETING ADAPTIVE IMMUNITY? IS THIS THE CAUSE OF SHINGLES, FOR EXAMPLE?
In a 2019 study, funded in part by the Gates foundation, it was discovered that the measles virus causes the body to "forget" its immune response to previously encountered pathogens.
Lectins enhance SARS-CoV-2 infection and influence neutralizing antibodies (2021)
âConversely, antibodies to the receptor binding motif, while potently neutralizing infection of ACE2-overexpressing cells, poorly neutralize infection of cells expressing DC-SIGN or L-SIGN and trigger fusogenic rearrangement of the spike, promoting cell-to-cell fusion. Collectively, these findings identify a lectin-dependent pathway that enhances ACE2-dependent infection by SARS-CoV-2 and reveal distinct mechanisms of neutralization by different classes of spike-specific antibodies.â
Abstract
SARS-CoV-2 infectionâwhich involves both cell attachment and membrane fusionârelies on the angiotensin-converting enzyme 2 (ACE2) receptor, which is paradoxically found at low levels in the respiratory tract1,2,3, suggesting that there may be additional mechanisms facilitating infection. Here we show that C-type lectin receptors, DC-SIGN, L-SIGN and the sialic acidâbinding immunoglobulin-like lectin 1 (SIGLEC1) function as attachment receptors by enhancing ACE2-mediated infection and modulating the neutralizing activity of different classes of spike-specific antibodies. Antibodies to the amino-terminal domain or to the conserved site at the base of the receptor-binding domain, while poorly neutralizing infection of ACE2-overexpressing cells, effectively block lectin-facilitated infection. Conversely, antibodies to the receptor binding motif, while potently neutralizing infection of ACE2-overexpressing cells, poorly neutralize infection of cells expressing DC-SIGN or L-SIGN and trigger fusogenic rearrangement of the spike, promoting cell-to-cell fusion. Collectively, these findings identify a lectin-dependent pathway that enhances ACE2-dependent infection by SARS-CoV-2 and reveal distinct mechanisms of neutralization by different classes of spike-specific antibodies.
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Spike protein (inc vax) induced immunodeficiency & carcinogenesis megathread #11: Lectins enhance SARS-CoV-2 infection and influence neutralizing antibodies
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Any extracts used in the following article are for non commercial research and educational purposes only and may be subject to copyright from their respective owners.
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1) IS THE SPIKE PROTEIN DELETING ADAPTIVE IMMUNITY? IS THIS THE CAUSE OF SHINGLES, FOR EXAMPLE?
In a 2019 study, funded in part by the Gates foundation, it was discovered that the measles virus causes the body to "forget" its immune response to previously encountered pathogens.
https://threadreaderapp.com/thread/1396290652015562762.html
Lectins enhance SARS-CoV-2 infection and influence neutralizing antibodies (2021)
âConversely, antibodies to the receptor binding motif, while potently neutralizing infection of ACE2-overexpressing cells, poorly neutralize infection of cells expressing DC-SIGN or L-SIGN and trigger fusogenic rearrangement of the spike, promoting cell-to-cell fusion. Collectively, these findings identify a lectin-dependent pathway that enhances ACE2-dependent infection by SARS-CoV-2 and reveal distinct mechanisms of neutralization by different classes of spike-specific antibodies.â
Abstract
SARS-CoV-2 infectionâwhich involves both cell attachment and membrane fusionârelies on the angiotensin-converting enzyme 2 (ACE2) receptor, which is paradoxically found at low levels in the respiratory tract1,2,3, suggesting that there may be additional mechanisms facilitating infection. Here we show that C-type lectin receptors, DC-SIGN, L-SIGN and the sialic acidâbinding immunoglobulin-like lectin 1 (SIGLEC1) function as attachment receptors by enhancing ACE2-mediated infection and modulating the neutralizing activity of different classes of spike-specific antibodies. Antibodies to the amino-terminal domain or to the conserved site at the base of the receptor-binding domain, while poorly neutralizing infection of ACE2-overexpressing cells, effectively block lectin-facilitated infection. Conversely, antibodies to the receptor binding motif, while potently neutralizing infection of ACE2-overexpressing cells, poorly neutralize infection of cells expressing DC-SIGN or L-SIGN and trigger fusogenic rearrangement of the spike, promoting cell-to-cell fusion. Collectively, these findings identify a lectin-dependent pathway that enhances ACE2-dependent infection by SARS-CoV-2 and reveal distinct mechanisms of neutralization by different classes of spike-specific antibodies.
Full version:
https://www.nature.com/articles/s41586-021-03925-1
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