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Posted On: 07/27/2021 5:36:36 PM
Post# of 153878
I apologize if this has been adddressed previously.
However, interesting reports indicating that long Covid likely, at least in part, due to EBV reactivation.
https://bioengineer.org/long-covid-symptoms-l...ctivation/
“ Long COVID symptoms likely caused by Epstein-Barr virus reactivation”
“ The researchers then found, in a subset of 68 COVID-19 patients randomly selected from those surveyed, that 66.7% of long COVID subjects versus 10% of controls were positive for EBV reactivation based on positive EBV early antigen-diffuse (EA-D) IgG or EBV viral capsid antigen (VCA) IgM titers. The difference was significant ”
I’ve been digging trying to appreciate the steps in EBV reactivation and found this:
The presence of functional CCR5 and EBV reactivation after allogeneic haematopoietic stem cell transplantation
The incidence of EBV reactivation 2-3 months after transplantation was significantly lower in patients carrying the CCR5Delta32 allele (P=0.008)
https://pubmed.ncbi.nlm.nih.gov/17530006/
While addressing cancer rather than Covid, it appears that ENV reactivation is CCl5/CCR5 mediated.
https://www.onlinelibrary.wiley.com/doi/10.1111/cas.13584
“ Induction of chemokine (C-C motif) ligand 5 by Epstein–Barr virus infection enhances tumor angiogenesis in nasopharyngeal carcinoma”
“ Subsequent proteomic analysis revealed that EBV infection increased the expression of a series of angiogenic factors, including chemokine (C-C motif) ligand 5 (CCL5). We then proved that CCL5 was a target of EBV in inducing tumor angiogenesis and growth. Further investigation through transcriptome analysis indicated that the pro-angiogenic function of CCL5 might be mediated by the PI3K/AKT pathway. Furthermore, we confirmed that activation of the PI3K/AKT and hypoxia-inducible factor-1α pathways was essential for CCL5-promoted angiogenesis.”
I am sure Ohm20 can explain the details. I don’t expect to understand the PI3K/AKT/MTor pathway for a long while, but nonetheless found it exciting to see that EBV reactivation is likely a large part of LH/PASC and that Leronlimab is likely a (the?) solution.
However, interesting reports indicating that long Covid likely, at least in part, due to EBV reactivation.
https://bioengineer.org/long-covid-symptoms-l...ctivation/
“ Long COVID symptoms likely caused by Epstein-Barr virus reactivation”
“ The researchers then found, in a subset of 68 COVID-19 patients randomly selected from those surveyed, that 66.7% of long COVID subjects versus 10% of controls were positive for EBV reactivation based on positive EBV early antigen-diffuse (EA-D) IgG or EBV viral capsid antigen (VCA) IgM titers. The difference was significant ”
I’ve been digging trying to appreciate the steps in EBV reactivation and found this:
The presence of functional CCR5 and EBV reactivation after allogeneic haematopoietic stem cell transplantation
The incidence of EBV reactivation 2-3 months after transplantation was significantly lower in patients carrying the CCR5Delta32 allele (P=0.008)
https://pubmed.ncbi.nlm.nih.gov/17530006/
While addressing cancer rather than Covid, it appears that ENV reactivation is CCl5/CCR5 mediated.
https://www.onlinelibrary.wiley.com/doi/10.1111/cas.13584
“ Induction of chemokine (C-C motif) ligand 5 by Epstein–Barr virus infection enhances tumor angiogenesis in nasopharyngeal carcinoma”
“ Subsequent proteomic analysis revealed that EBV infection increased the expression of a series of angiogenic factors, including chemokine (C-C motif) ligand 5 (CCL5). We then proved that CCL5 was a target of EBV in inducing tumor angiogenesis and growth. Further investigation through transcriptome analysis indicated that the pro-angiogenic function of CCL5 might be mediated by the PI3K/AKT pathway. Furthermore, we confirmed that activation of the PI3K/AKT and hypoxia-inducible factor-1α pathways was essential for CCL5-promoted angiogenesis.”
I am sure Ohm20 can explain the details. I don’t expect to understand the PI3K/AKT/MTor pathway for a long while, but nonetheless found it exciting to see that EBV reactivation is likely a large part of LH/PASC and that Leronlimab is likely a (the?) solution.
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