I hesitate to try and characterize the reference below because it is not terribly clear, but I think (??) it tends to support your point that the newer variants may already escape XBB induced immunity.
Thank you for sharing that link. I have been looking for a study on EG.5.1. My suspicion of it being able to effectively evade antibodies from prior infections, including from earlier XBB lineages is accurate. This study doesn't get into showing a greater ability to break down the mucosal epithelium but that is still expected until it is shown otherwise because it has so many of the Delta variant mutations. Prepare for the worst but hope for the best.
Sadly, this means that the new vaccines that target XBB variants will not stop transmission and will require us to use our finite amount of naive T-cells to eliminate the virus from our bodies, also further exhausting circulating T-cells. This process stresses out the thymus, and the virus can potential infect the thymus causing long-term damage to the immune system. This is especially dangerous in young children and older adults. The vaccines may provide a benefit to anyone that hasn't been infected by any of the XBB variants by boosting T-cell response but I suspect very few people haven't already been exposed to any of the XBB variants. Most people likely had a least a low dose exposure already, which would have had the same effect.
Further, relying on T-cells stresses out the liver and kidneys. The virus will still have time to spread throughout the body, infecting multiple organs, including potentially the brain.
The viral load exposed to will have a direct impact on how serious infections are. Increasing mitigation measures is necessary to limit exposure to this variant.
The paper shows, that, "EG.5.1 exhibits a higher effective reproduction number compared with XBB.1.5, XBB.1.16, and its parental lineage (XBB.1.9.2), suggesting that EG.5.1 will spread globally and outcompete these XBB subvariants in the near future."
Since you mentioned T-Cells being stressed, I thought I would pass along this reference if you haven't seen it. The findings suggest chronic T-cell activation in SARS-CoV-2 infected individuals. File this under the 'Real Bad' category. T-cell exhaustion does not lead to happy endings.
Thanks for the link! Persistence for two years and likely for life in many people like EBV, Herpes, and AIDS .
Here's a few of the older studies showing that we have known this yet public health does nothing to help people to understand whats going on or provide the guidance that would protect people.
Published: 19 March 2020
Functional exhaustion of antiviral lymphocytes in COVID-19 patients
A comparable reduction in B cells and a more severe reduction in the total amount of T cells in COVID as compared to AIDS. The total numbers of T cells, in particular of the CD8+ subpopulation, are lower in COVID than with AIDS, while the CD4+ are reduced in both.
COVID & AIDS are the leading cause of lymphocytopenia. This increases recurrent viral, bacterial or fungal infections and also increases the odds of cancers and autoimmune disorders.
"Immune cell dysregulation is a driver of COVID severity" (peer-reviewed)
"decreased total conventional DC (cDC), conventional type 2 DC (DC2), and plasmacytoid DC (pDC). CyTOF also showed lymphopenia of CD4 and CD8 T cell populations"
ACE2-independent infection of T lymphocytes by SARS-CoV-2"
"This work confirmed a SARS-CoV-2 infection of T cells, in a spike-ACE2-independent manner, which shed novel insights into the underlying mechanisms of SARS-CoV-2-induced lymphopenia in COVID."
SARS-CoV-2 Uses CD4 to Infect T Helper Lymphocytes
"Once inside T helper cells, SARS-CoV-2 assembles viral factories, impairs cell function and may cause cell death. SARS-CoV-2 infected T helper cells express higher amounts of IL-10, which is associated with viral persistence and disease severity. Thus, CD4-mediated SARS-CoV-2 infection of T helper cells may explain the poor adaptive immune response of many COVID-19 patients."
SARS-CoV-2 Dysregulates Neutrophil Degranulation and Reduces Lymphocyte Counts
" SARS-CoV-2-infected neutrophils had a direct effect on peripheral blood lymphocyte counts, with decreasing numbers of CD19+ B cells, CD8+ T cells, and CD4+ T cells. Together, this study highlights the independent role of neutrophils in contributing to the aberrant immune responses observed during SARS-CoV-2 infection that may be further dysregulated in the presence of other immune cells
"SARS-CoV-2-infected neonates had lower hemoglobin, neutrophil to lymphocyte ratio, total white blood cell count, and absolute neutrophil count compared to noninfected babies."
Wow...thanks for that masterful summary. If you're not concerned after seeing that, you're not paying attention. The plethora of denial is simply staggering.
Is this the correct reference for this statement? I simply don't see it in THIS reference. But I believe I have seen the statement, maybe in the Brazilian paper that looked at pathology from kids who had COVID and later had their tonsils & adenoids removed???
Please don't feel the need to chase this down!!! Maybe I'm just missing it.
"The total numbers of T cells, in particular of the CD8+ subpopulation, are lower in COVID than with AIDS, while the CD4+ are reduced in both."
Hi TACT...
I hesitate to try and characterize the reference below because it is not terribly clear, but I think (??) it tends to support your point that the newer variants may already escape XBB induced immunity.
https://www.biorxiv.org/content/10.1101/2023.08.08.552415v1
Thank you for sharing that link. I have been looking for a study on EG.5.1. My suspicion of it being able to effectively evade antibodies from prior infections, including from earlier XBB lineages is accurate. This study doesn't get into showing a greater ability to break down the mucosal epithelium but that is still expected until it is shown otherwise because it has so many of the Delta variant mutations. Prepare for the worst but hope for the best.
Sadly, this means that the new vaccines that target XBB variants will not stop transmission and will require us to use our finite amount of naive T-cells to eliminate the virus from our bodies, also further exhausting circulating T-cells. This process stresses out the thymus, and the virus can potential infect the thymus causing long-term damage to the immune system. This is especially dangerous in young children and older adults. The vaccines may provide a benefit to anyone that hasn't been infected by any of the XBB variants by boosting T-cell response but I suspect very few people haven't already been exposed to any of the XBB variants. Most people likely had a least a low dose exposure already, which would have had the same effect.
Further, relying on T-cells stresses out the liver and kidneys. The virus will still have time to spread throughout the body, infecting multiple organs, including potentially the brain.
The viral load exposed to will have a direct impact on how serious infections are. Increasing mitigation measures is necessary to limit exposure to this variant.
The paper shows, that, "EG.5.1 exhibits a higher effective reproduction number compared with XBB.1.5, XBB.1.16, and its parental lineage (XBB.1.9.2), suggesting that EG.5.1 will spread globally and outcompete these XBB subvariants in the near future."
Hi TACT...
Since you mentioned T-Cells being stressed, I thought I would pass along this reference if you haven't seen it. The findings suggest chronic T-cell activation in SARS-CoV-2 infected individuals. File this under the 'Real Bad' category. T-cell exhaustion does not lead to happy endings.
https://www.medrxiv.org/content/10.1101/2023.07.27.23293177v1.full.pdf
Thanks for the link! Persistence for two years and likely for life in many people like EBV, Herpes, and AIDS .
Here's a few of the older studies showing that we have known this yet public health does nothing to help people to understand whats going on or provide the guidance that would protect people.
Published: 19 March 2020
Functional exhaustion of antiviral lymphocytes in COVID-19 patients
https://www.nature.com/articles/s41423-020-0402-2
"SARS-CoV-2 and HIV-1: So Different yet so Alike. Immune Response at the Cellular and Molecular Level"
https://www.medsci.org/v19p1787.htm
A comparable reduction in B cells and a more severe reduction in the total amount of T cells in COVID as compared to AIDS. The total numbers of T cells, in particular of the CD8+ subpopulation, are lower in COVID than with AIDS, while the CD4+ are reduced in both.
https://www.nature.com/articles/s41590-021-01113-x?s=09
COVID & AIDS are the leading cause of lymphocytopenia. This increases recurrent viral, bacterial or fungal infections and also increases the odds of cancers and autoimmune disorders.
https://www.msdmanuals.com/professional/hematology-and-oncology/leukopenias/lymphocytopenia
"Immune cell dysregulation is a driver of COVID severity" (peer-reviewed)
"decreased total conventional DC (cDC), conventional type 2 DC (DC2), and plasmacytoid DC (pDC). CyTOF also showed lymphopenia of CD4 and CD8 T cell populations"
https://www.eurekalert.org/news-releases/966773
ACE2-independent infection of T lymphocytes by SARS-CoV-2"
"This work confirmed a SARS-CoV-2 infection of T cells, in a spike-ACE2-independent manner, which shed novel insights into the underlying mechanisms of SARS-CoV-2-induced lymphopenia in COVID."
https://www.nature.com/articles/s41392-022-00919-x
SARS-CoV-2 Uses CD4 to Infect T Helper Lymphocytes
"Once inside T helper cells, SARS-CoV-2 assembles viral factories, impairs cell function and may cause cell death. SARS-CoV-2 infected T helper cells express higher amounts of IL-10, which is associated with viral persistence and disease severity. Thus, CD4-mediated SARS-CoV-2 infection of T helper cells may explain the poor adaptive immune response of many COVID-19 patients."
https://www.medrxiv.org/content/10.1101/2020.09.25.20200329v1
SARS-CoV-2 Dysregulates Neutrophil Degranulation and Reduces Lymphocyte Counts
" SARS-CoV-2-infected neutrophils had a direct effect on peripheral blood lymphocyte counts, with decreasing numbers of CD19+ B cells, CD8+ T cells, and CD4+ T cells. Together, this study highlights the independent role of neutrophils in contributing to the aberrant immune responses observed during SARS-CoV-2 infection that may be further dysregulated in the presence of other immune cells
https://www.mdpi.com/2227-9059/10/2/382
"SARS-CoV-2-infected neonates had lower hemoglobin, neutrophil to lymphocyte ratio, total white blood cell count, and absolute neutrophil count compared to noninfected babies."
https://www.cureus.com/articles/90918-comparison-of-hematological-and-biochemical-parameters-of-sars-cov-2-positive-and--negative-neonates-of-covid-19-mothers-in-a-covid-19-hospital-odisha-state
Wow...thanks for that masterful summary. If you're not concerned after seeing that, you're not paying attention. The plethora of denial is simply staggering.
TACT...
Is this the correct reference for this statement? I simply don't see it in THIS reference. But I believe I have seen the statement, maybe in the Brazilian paper that looked at pathology from kids who had COVID and later had their tonsils & adenoids removed???
Please don't feel the need to chase this down!!! Maybe I'm just missing it.
"The total numbers of T cells, in particular of the CD8+ subpopulation, are lower in COVID than with AIDS, while the CD4+ are reduced in both."
https://www.nature.com/articles/s41590-021-01113-x?s=09