This article highlights a new study showing that Nirmatrelvil, the active ingredient in Paxlovid, prevents an adequate adaptive immune response to the SARS-CoV-2 virus.
In the study, the SARS-CoV-2-infected mice failed to develop antibodies, memory T cells, and B cells specific to SARS-CoV-2 on initial and second exposure to the virus.
The K18-hACE2 mice used in the study are genetically modified to have human ACE2 receptors. The SARS-CoV-2 virus uses ACE2 receptors to enter human cells and start COVID-19.
Adaptive Immune Response
As a background, the body has an innate and adaptive immune system. The innate immune system provides the initial response to an infection and activates the adaptive immune system.
The adaptive immune system makes antibodies and lymphocytes specific to a particular pathogen. However, it may take days or weeks before they are made. But it can be made shorter.
After the initial exposure to the virus, the adaptive immune system retains the “template” of the specific antibodies and specialized lymphocytes (memory T cells and B cells) so that the adaptive response becomes faster on subsequent exposure.
The investigators treated the mice six times with nirmatrelvir starting four hours post-infection and every 12 hours after that up until day three post-infection.
Results
The nirmatrelvir-treated SARS-CoV-2 infected mice showed virtually undetectable viral RNA and infectious virus. The significance of this finding concerning the adaptive immune response will be discussed below.
Mice treated with nirmatrelvir have reduced antibodies to the S1 subunit of the spike protein and the Omicron variant at 14 and 21 days post-infection, respectively, and four days after the re-challenge.
Aside from that, the B cells recovered from nirmatrelvir-treated mice four days after re-challenge exhibited a lower expression of the activation marker CD95.
CD95 is needed to recruit T-cells in the inflamed area and eliminate infected and damaged cells.
What happened to the adaptive immune response?
As mentioned earlier, the nirmatrelvir-treated mice had undetectable viral RNA and infectious viruses. That may sound good, but it may be double-edged.
Due to the elimination of the virus, the adaptive immune system did not have enough “material” to pattern the templates for the antibodies and lymphocytes.
Although the mechanistic bases behind this observation were not addressed in this study, it is conceivable that this is due to insufficient antigen exposure (quantity and/or duration) of naïve B and T cells.
Could the nirmatrelvir affect the entire adaptive immune system?
Is the Paxlovid an immune suppresant? To answer this, the study infected mice with the vesicular stomatitis virus and lymphocytic choriomeningitis virus and treated them with nirmatrelvir.
The results this time showed the proper development of an adaptive immune response. To the authors, this suggests that nirmatrelvir is not an immune suppressive drug.
In summary, Paxlovid blunts the antiviral adaptive immune response in SARS-CoV-2 infected mice.
The study is available in preprint and has not been peer-reviewed. I think it is well made, IMHO. It is available HERE.
The authors are from The Division of Immunology, Transplantation, and Infectious Diseases, IRCCS San Raffaele Scientific Institute, University of Naples, Cittadella Universitaria di Monserrato and other institutions in Italy.
The study may explain why many people like Anthony Fauci, Joe Biden, and CDC Director Rochelle Walensky, who took Paxlovid, have rebound COVID. I discussed the study about that at:
Don’t Get Sick!
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