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Posted On: 04/25/2022 10:21:32 PM
Post# of 148899
If you want to see a few more details on the Clinical Infectious Disease report (where only the abstract can be seen), go to Cytodyn's "Publications" webpage (link below) and click the top report dated 4/22/2022.
https://www.cytodyn.com/publications
A 3-page "Brief Report" from Clinical Infectious Diseases will pop up. It has a little more info than the abstract previously discussed. If you click any of the Supplementary Tables in the Brief Report, you will be taken to the page with the abstract and will not be able to see the tables.
There is, however, a little more discussion than is given in the abstract. Here is an excerpt from the Brief Report.
DISCUSSION
These findings suggest an unexpected alternative mechanism for long COVID. Rather than persistent immune activation, we observed abnormal immune downmodulation, which is normalized by leronlimab. We hypothesize that this could be immune overshoot after the intense inflammation in acute COVID-19. With genetic polymorphisms reducing cell surface CCR5 levels conferring increased risk of severe COVID-19 [4], this suggests a complex role for CCR5 in balancing inflammatory and antiinflammatory effects, for example, through T regulatory cells. While leronlimab reduces the signaling of CCR5 by Regulated upon Activation, Normal T Cell Expressed and Presumably Secreted (RANTES) [11], emerging data show that leronlimab stabilizes CCR5 expression, presumably through direct binding [12, 13], which may either change the signaling or activity of other ligands, such as Monocyte Inflammatory Protein (MIP)-1ɑ, MIP-1β, and/or Monocyte Chemoattractant Protein (MCP-2), or increase the expression of other CCRs through heterodimerization [14]. While this is a small exploratory pilot study with potential confounders, our results support further research into the role of CCR5 in long COVID.
https://www.cytodyn.com/publications
A 3-page "Brief Report" from Clinical Infectious Diseases will pop up. It has a little more info than the abstract previously discussed. If you click any of the Supplementary Tables in the Brief Report, you will be taken to the page with the abstract and will not be able to see the tables.
There is, however, a little more discussion than is given in the abstract. Here is an excerpt from the Brief Report.
DISCUSSION
These findings suggest an unexpected alternative mechanism for long COVID. Rather than persistent immune activation, we observed abnormal immune downmodulation, which is normalized by leronlimab. We hypothesize that this could be immune overshoot after the intense inflammation in acute COVID-19. With genetic polymorphisms reducing cell surface CCR5 levels conferring increased risk of severe COVID-19 [4], this suggests a complex role for CCR5 in balancing inflammatory and antiinflammatory effects, for example, through T regulatory cells. While leronlimab reduces the signaling of CCR5 by Regulated upon Activation, Normal T Cell Expressed and Presumably Secreted (RANTES) [11], emerging data show that leronlimab stabilizes CCR5 expression, presumably through direct binding [12, 13], which may either change the signaling or activity of other ligands, such as Monocyte Inflammatory Protein (MIP)-1ɑ, MIP-1β, and/or Monocyte Chemoattractant Protein (MCP-2), or increase the expression of other CCRs through heterodimerization [14]. While this is a small exploratory pilot study with potential confounders, our results support further research into the role of CCR5 in long COVID.
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