sharon sanders
Editor-in-Chief & President
Biomedical Journal
Volume 47, Issue 3, June 2024,
100650
Acquired Immune Deficiency Syndrome correlation with SARS-CoV-2 N genotypes
Author links open overlay panelIñigo Ximeno-Rodríguez [SUP]a[/SUP], Irene Blanco-delRío [SUP]a[/SUP], Egoitz Astigarraga [SUP]b[/SUP], Gabriel Barreda-Gómez [SUP]b[/SUP]
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https://doi.org/10.1016/j.bj.2023.100650Get rights and content
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Highlights
Background
Epigenetics and clinical observations referring to Betacoronavirus lead to the conjecture that Sarbecovirus may have the ability to infect lymphocytes using a different way than the spike protein. In addition to inducing the death of lymphocytes, thus drastically reducing their population and causing a serious immune deficiency, allows it to remain hidden for long periods of latency using them as a viral reservoir in what is named Long-Covid Disease. Exploring possibilities, the hypothesis is focused on that N protein may be the key of infecting lymphocytes.
Method
The present article exhibits a computational assay for the latest complete sequences reported to GISAID, correlating N genotypes with an enhancement in the affinity of the complex that causes immune deficiency in order to determine a good docking with the N protein and some receptors in lymphocytes.
Results
A novel high-interaction coupling of N-RBD and CD147 is presented as the main way of infecting lymphocytes, allowing to define those genotypes involved in their affinity enhancement.
Conclusion
The hypothesis is consistent with the mutagenic deriving observed on the in-silico assay, which reveals that genotypes N/120 and N/152 are determinant to reduce the Immune Response of the host infecting lymphocytes, allowing the virus persists indefinitely and causing an Acquire Immune Deficiency Syndrome.
https://www.sciencedirect.com/science/article/pii/S2319417023000872
Volume 47, Issue 3, June 2024,
100650
Acquired Immune Deficiency Syndrome correlation with SARS-CoV-2 N genotypes
Author links open overlay panelIñigo Ximeno-Rodríguez [SUP]a[/SUP], Irene Blanco-delRío [SUP]a[/SUP], Egoitz Astigarraga [SUP]b[/SUP], Gabriel Barreda-Gómez [SUP]b[/SUP]
Show more
Add to Mendeley
Share
Cite
https://doi.org/10.1016/j.bj.2023.100650Get rights and content
Under a Creative Commons license
Open access
Highlights
- •
Genotypes N/120 and N/152 of SARS-CoV-2 have been identified in the acquired immuno-deficiency scope caused by Sarbecovirus. - •
A new binding site for the Sarbecovirus N protein is proposed as the main route of infection of lymphocytes through CD147 receptors. - •
Immune dysregulation caused by infection of CD147 lymphocytes is consistent with clinical data of severe and Long Covid cases.
Background
Epigenetics and clinical observations referring to Betacoronavirus lead to the conjecture that Sarbecovirus may have the ability to infect lymphocytes using a different way than the spike protein. In addition to inducing the death of lymphocytes, thus drastically reducing their population and causing a serious immune deficiency, allows it to remain hidden for long periods of latency using them as a viral reservoir in what is named Long-Covid Disease. Exploring possibilities, the hypothesis is focused on that N protein may be the key of infecting lymphocytes.
Method
The present article exhibits a computational assay for the latest complete sequences reported to GISAID, correlating N genotypes with an enhancement in the affinity of the complex that causes immune deficiency in order to determine a good docking with the N protein and some receptors in lymphocytes.
Results
A novel high-interaction coupling of N-RBD and CD147 is presented as the main way of infecting lymphocytes, allowing to define those genotypes involved in their affinity enhancement.
Conclusion
The hypothesis is consistent with the mutagenic deriving observed on the in-silico assay, which reveals that genotypes N/120 and N/152 are determinant to reduce the Immune Response of the host infecting lymphocytes, allowing the virus persists indefinitely and causing an Acquire Immune Deficiency Syndrome.
https://www.sciencedirect.com/science/article/pii/S2319417023000872