This is an interesting idea but would benefit from more elaboration.
Why the GI tract in particular—do you have evidence that this will significantly reduce the risk of respiratory symptoms, or just speculation / “common sense”? Is there evidence that the GI tract as the initial site of exposure will produce an infection / an immune response, but with a reduced chance of the infection spreading to the lungs / respiratory tract? Or with it taking longer to get there, similar to Robin Hanson’s thoughts about deliberate exposure with a low dose, like variolation of old?
If you have any links/references, please definitely post them. If it’s just speculation, it’s interesting speculation but tell us what it’s based on.
Exactly like variolation, except you do it intelligently to minimize lung infection.
SARS and SARS-Cov2 are both ACE2 dependent for cell entry.
ACE2 expression in AT2 cells in the lower respiratory track is known to be on the apical surface, that is the side of the cell facing airspace, not the basal surface facing vasculature. Hypothesis would be that lung infection is much more efficient and virulent by droplet delivery rather than by virus circulating in blood stream. I am also under the understanding that the kidney and heart complications are due to poor oxygenation due to the respiratory distress, not a primary viremia in those organs.
Tissue distribution of ACE2 protein, the functional receptor for SARS coronavirus. A first step in understanding SARS pathogenesis.
“In conclusion, ACE2 is abundantly present in humans in the epithelia of the lung and small intestine, which might provide possible routes of entry for the SARS-CoV. ”
ACE2 expression by colonic epithelial cells is associated with viral infection, immunity and energy metabolism
“Studies have identified the SARS-CoV-2 RNA in stool specimens of infected patients, and its viral receptor angiotensin converting enzyme 2 (ACE2) was found to be highly expressed in gastrointestinal epithelial cells. These suggest that SARS-CoV-2 can actively infect and replicate in the gastrointestinal tract. This has important implications to the disease management, transmission, and infection control.”
Severe acute respiratory syndrome and its lesions in digestive system
Cool, thanks for expanding on that. You might want to link this comment in your other comments about this idea, so people have some details to read. It’s a lot more informative than the one I was responding to!
Innoculate GI tract with live virus. Suffer GI symptoms. Get immunity. Avoid respiratory complications.
This is an interesting idea but would benefit from more elaboration.
Why the GI tract in particular—do you have evidence that this will significantly reduce the risk of respiratory symptoms, or just speculation / “common sense”? Is there evidence that the GI tract as the initial site of exposure will produce an infection / an immune response, but with a reduced chance of the infection spreading to the lungs / respiratory tract? Or with it taking longer to get there, similar to Robin Hanson’s thoughts about deliberate exposure with a low dose, like variolation of old?
If you have any links/references, please definitely post them. If it’s just speculation, it’s interesting speculation but tell us what it’s based on.
Exactly like variolation, except you do it intelligently to minimize lung infection.
SARS and SARS-Cov2 are both ACE2 dependent for cell entry.
ACE2 expression in AT2 cells in the lower respiratory track is known to be on the apical surface, that is the side of the cell facing airspace, not the basal surface facing vasculature. Hypothesis would be that lung infection is much more efficient and virulent by droplet delivery rather than by virus circulating in blood stream. I am also under the understanding that the kidney and heart complications are due to poor oxygenation due to the respiratory distress, not a primary viremia in those organs.
https://www.ncbi.nlm.nih.gov/pubmed/15141377
Tissue distribution of ACE2 protein, the functional receptor for SARS coronavirus. A first step in understanding SARS pathogenesis.
“In conclusion, ACE2 is abundantly present in humans in the epithelia of the lung and small intestine, which might provide possible routes of entry for the SARS-CoV. ”
ACE2 expression by colonic epithelial cells is associated with viral infection, immunity and energy metabolism
https://www.medrxiv.org/content/10.1101/2020.02.05.20020545v1.full.pdf
The digestive system is a potential route of 2019-nCov infection: a bioinformatics analysis based on single-cell transcriptomes
https://www.biorxiv.org/content/10.1101/2020.01.30.927806v1.full.pdf
Covid-19 and the Digestive System.
https://www.ncbi.nlm.nih.gov/pubmed/32215956
“Studies have identified the SARS-CoV-2 RNA in stool specimens of infected patients, and its viral receptor angiotensin converting enzyme 2 (ACE2) was found to be highly expressed in gastrointestinal epithelial cells. These suggest that SARS-CoV-2 can actively infect and replicate in the gastrointestinal tract. This has important implications to the disease management, transmission, and infection control.”
Severe acute respiratory syndrome and its lesions in digestive system
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4611772/
Cool, thanks for expanding on that. You might want to link this comment in your other comments about this idea, so people have some details to read. It’s a lot more informative than the one I was responding to!
Neat idea, although immune responses can be tissue specific (to a certain degree).