4 ms·

I suspect it's because this virus is optimized to enter cells that line the lungs/respiratory tract, then also sheds back that same way. Meanwhile, cells in, an

by gojomo 7y ago

I suspect it's because this virus is optimized to enter cells that line the lungs/respiratory tract, then also sheds back that same way. Meanwhile, cells in, and along, the bloodstream aren't infected – and are most-trafficked by the body's immune response, including virus-destroying antibodies. (Why are rodents more prevalent in the walls/crawlspaces of a dwelling, rather than the hallways?)

hinkley 7y ago
But the lungs are full of blood, that's how we breath. So it's spreading mucosally or through connective tissue?
- gojomo 7y ago
  Sure, but if an initially-infected respiratory cell releases its "baby coronaviruses" out to the respiratory linings, away from the blood, they'll find lots more of the respiratory cell surfaces they're optimized to infect, and maybe get a ride out to other hosts on sputum. To the extent an infected cell releases its "baby coronaviruses" into the blood stream, they find a hot, chemically active environment – which is already inhospitable to their continued survival – plus a relative dearth of the respiratory cell-walls they're optimized to enter, plus a growing number of hostile antibodies. (I don't know if a coronavirus-hijacked cell can direct its fresh viruses one way or the other, but it'd probably prefer to do that if it could, and I can understand why viruses wouldn't persist long in blood compared to respiratory-membranes.) The coronaviruses are definitely active in mucosal surfaces, and carried by mucus. I haven't seen anything about, nor do I think any activity is necessarily implied, in other connective tissues.
- dmm10 7y ago
  As far as I know the route of SARS-Cov-2 spreading in the human body isn't known beyond the change in locality of symptomatic expression with progression of Covid-19 (upper respiratory tract to lower respiratory tract.) Research has shown (1) the distribution of ACE2 protein, the functional receptor for SARS-Cov and SARS-Cov-2 (2), to include various human organs (oral and nasal mucosa, nasopharynx, lung, stomach, small intestine, colon, skin, lymph nodes, thymus, bone marrow, spleen, liver, kidney, and brain) along with arterial and venous endothelial cells and arterial smooth muscle cells in all organs studied. And ACE2 mRNA has been found in virtually all organs. So there is definitely the potential for cells in the circulatory system binding viruses. What may be significant here is the concentration of ACE2 protein in cell membranes. One Chinese analysis of a group of 170 Covid-19 fatalities(3) found half of the cases suffered from hypertension. ACE inhibitors are a class of medication prescribed for lowering blood pressure and according to models they increase the concentration of ACE2 protein in lower respiratory tract cells. Given that fatality results from respiratory distress originating in the lower respiratory tract and that not all cases progress to the lower respiratory tract it seems possible that the spread of the virus within the body may be related to concentration of ACE2 protein in cells. The disease progression would also support mucosal transport of the virus within individuals the same as between them. (1) Tissue distribution of ACE2 protein, the functional receptor for SARS coronavirus. A first step in understanding SARS pathogenesis. https://www.ncbi.nlm.nih.gov/pubmed/15141377 https://www.ncbi.nlm.nih.gov/pubmed/15141377 (2) Structure, Function, and Antigenicity of the SARS-CoV-2 Spike Glycoprotein https://www.sciencedirect.com/science/article/pii/S0092867420302622 https://www.sciencedirect.com/science/article/pii/S009286742... (3) Controversial Study Links COVID-19 Severity to ACEIs and ARBs (Newsweek, March 24, 2020)

by gojomo 7y ago

hinkley 7y ago

But the lungs are full of blood, that's how we breath. So it's spreading mucosally or through connective tissue?

gojomo 7y ago
Sure, but if an initially-infected respiratory cell releases its "baby coronaviruses" out to the respiratory linings, away from the blood, they'll find lots more of the respiratory cell surfaces they're optimized to infect, and maybe get a ride out to other hosts on sputum. To the extent an infected cell releases its "baby coronaviruses" into the blood stream, they find a hot, chemically active environment – which is already inhospitable to their continued survival – plus a relative dearth of the respiratory cell-walls they're optimized to enter, plus a growing number of hostile antibodies. (I don't know if a coronavirus-hijacked cell can direct its fresh viruses one way or the other, but it'd probably prefer to do that if it could, and I can understand why viruses wouldn't persist long in blood compared to respiratory-membranes.) The coronaviruses are definitely active in mucosal surfaces, and carried by mucus. I haven't seen anything about, nor do I think any activity is necessarily implied, in other connective tissues.
dmm10 7y ago
As far as I know the route of SARS-Cov-2 spreading in the human body isn't known beyond the change in locality of symptomatic expression with progression of Covid-19 (upper respiratory tract to lower respiratory tract.) Research has shown (1) the distribution of ACE2 protein, the functional receptor for SARS-Cov and SARS-Cov-2 (2), to include various human organs (oral and nasal mucosa, nasopharynx, lung, stomach, small intestine, colon, skin, lymph nodes, thymus, bone marrow, spleen, liver, kidney, and brain) along with arterial and venous endothelial cells and arterial smooth muscle cells in all organs studied. And ACE2 mRNA has been found in virtually all organs. So there is definitely the potential for cells in the circulatory system binding viruses. What may be significant here is the concentration of ACE2 protein in cell membranes. One Chinese analysis of a group of 170 Covid-19 fatalities(3) found half of the cases suffered from hypertension. ACE inhibitors are a class of medication prescribed for lowering blood pressure and according to models they increase the concentration of ACE2 protein in lower respiratory tract cells. Given that fatality results from respiratory distress originating in the lower respiratory tract and that not all cases progress to the lower respiratory tract it seems possible that the spread of the virus within the body may be related to concentration of ACE2 protein in cells. The disease progression would also support mucosal transport of the virus within individuals the same as between them. (1) Tissue distribution of ACE2 protein, the functional receptor for SARS coronavirus. A first step in understanding SARS pathogenesis. https://www.ncbi.nlm.nih.gov/pubmed/15141377 https://www.ncbi.nlm.nih.gov/pubmed/15141377 (2) Structure, Function, and Antigenicity of the SARS-CoV-2 Spike Glycoprotein https://www.sciencedirect.com/science/article/pii/S0092867420302622 https://www.sciencedirect.com/science/article/pii/S009286742... (3) Controversial Study Links COVID-19 Severity to ACEIs and ARBs (Newsweek, March 24, 2020)