ecstatichamster
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Chris Masterjohn Opposes RP's View On ACE2/COVID-19
- Thread starter yoshiesque
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Terma
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Ray's suggestion is more realistic and biological equivalent of "flattening the curve" if the measure is the amount of injury ("cell deaths" if you want a little fun). I assume the infection might persist longer but the symptoms have better chance to remain under the threshold for irreversible. If I had to accept something at a hospital besides i.v. ascorbate it's what I would try (any reason not to do them together? I saw no interactions on the internet...), however I'd be tempted to do it as needed based on symptom severity if it's fast-acting enough (sounds like it?), but I haven't read its pharmacodynamics. They'd prescribe it to me anyway. I think they had an even better idea with recombinent ACE2 but that sounds pricey.
Chris's way you would basically have to find individual inhibitors for all the downstream targets of AT receptor, though not impossible to cover a few; but some ACE2-promoting things also have anti-inflammatory effects through other channels, so I'm not sure that leaves you a winner. It's not totally stupid approach because it may be a good idea to have redundant therapies to lower cytokines, NOX (might take high doses of MB, though should be others) and others effectively even if you were talking losartan, which doesn't sound foolproof on its own? So to me it's just a question of hospital vs home that's 0:1 and not concerned enough to stop eating liver. Still I hope he recovers from that ***t didn't sound good.
Chris's way you would basically have to find individual inhibitors for all the downstream targets of AT receptor, though not impossible to cover a few; but some ACE2-promoting things also have anti-inflammatory effects through other channels, so I'm not sure that leaves you a winner. It's not totally stupid approach because it may be a good idea to have redundant therapies to lower cytokines, NOX (might take high doses of MB, though should be others) and others effectively even if you were talking losartan, which doesn't sound foolproof on its own? So to me it's just a question of hospital vs home that's 0:1 and not concerned enough to stop eating liver. Still I hope he recovers from that ***t didn't sound good.
freedom
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A Kahn Academy online course illustrates out how bad high levels of AngiotensinII are on the lungs, kidney, pancreas and other organs: Activating angiotensin 2 (video) | Khan Academy
The course also shows how Renin from the kidneys is the first step in producing ANGI while ACE is needed for ANGII. A graphic is helpful to visualize the pathway: https://www.frontiersin.org/files/Articles/96579/fphys-05-00227-HTML/image_m/fphys-05-00227-g001.jpg
Some ANGII is beneficial but too much could also be why the Corona virus becomes an issue:
Instead of messing around with ACE or ARB you could also reduce renin which would lower ANGI and ANGII. An inverse relation of the serum 1,25(OH)2D3 level to the plasma renin activity was observed in the following study:
The effects of vitamin D on the renin-angiotensin system
This is kind of a long winded video but it explains in great detail how the active form of vitD fights the Corona virus and references many other experts:
So sun, exercise (muscle contraction activates vitD) and oranges and we can all go back to work? : )
The course also shows how Renin from the kidneys is the first step in producing ANGI while ACE is needed for ANGII. A graphic is helpful to visualize the pathway: https://www.frontiersin.org/files/Articles/96579/fphys-05-00227-HTML/image_m/fphys-05-00227-g001.jpg
Some ANGII is beneficial but too much could also be why the Corona virus becomes an issue:
Instead of messing around with ACE or ARB you could also reduce renin which would lower ANGI and ANGII. An inverse relation of the serum 1,25(OH)2D3 level to the plasma renin activity was observed in the following study:
The effects of vitamin D on the renin-angiotensin system
This is kind of a long winded video but it explains in great detail how the active form of vitD fights the Corona virus and references many other experts:
So sun, exercise (muscle contraction activates vitD) and oranges and we can all go back to work? : )
Last edited:
S.Seneff
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ACE2 Expression is Increased in the Lungs of Patients with Comorbidities Associated with Severe COVID-19
Bruna GG Pinto, Antonio ER Oliveira, Youvika Singh, Leandro Jimenez, Andre NA Goncalves, Rodrigo LT Ogava, Rachel Creighton, Jean PS Peron, View ORCID ProfileHelder I Nakaya
doi: ACE2 Expression is Increased in the Lungs of Patients with Comorbidities Associated with Severe COVID-19
This article is a preprint and has not been peer-reviewed [what does this mean?]. It reports new medical research that has yet to be evaluated and so should not be used to guide clinical practice.
Highly ACE2 Expression in Pancreas May Cause Pancreas Damage After SARS-CoV-2 Infection
Furong Liu, Xin Long, Wenbin Zou, Minghao Fang, Wenjuan Wu, Wei Li, Bixiang Zhang, Wanguang Zhang, Xiaoping Chen, Zhanguo Zhang
doi: Highly ACE2 Expression in Pancreas May Cause Pancreas Damage After SARS-CoV-2 Infection
This article is a preprint and has not been peer-reviewed [what does this mean?]. It reports new medical research that has yet to be evaluated and so should not be used to guide clinical practice.
"We found ACE2 was expressed in many
organs or tissues except most brain tissues (Fig. 1A), which suggests that these organs
or tissues such as unreported ovary and thyroid might also be targets for SARS-CoV-2."
ACE2 expression by colonic epithelial cells is associated with viral infection, immunity and energy metabolism
Jun Wang, Shanmeizi Zhao, Ming Liu, Zhiyao Zhao, Yiping Xu, Ping Wang, Meng Lin, Yanhui Xu, Bing Huang, Xiaoyu Zuo, Zhanghua Chen, Fan Bai, Jun Cui, Andrew M Lew, Jincun Zhao, Yan Zhang, Haibin Luo, Yuxia Zhang
doi: ACE2 expression by colonic epithelial cells is associated with viral infection, immunity and energy metabolism
This article is a preprint and has not been peer-reviewed [what does this mean?]. It reports new medical research that has yet to be evaluated and so should not be used to guide clinical practice.
Paradoxically, although ACE2 mediates viral entry to the host, its deficiency worsens lung injury
by activating the renin-angiotensin system (RAS) in experimental models [6]. The circulating
RAS regulates blood pressure and fluid homeostasis. Local tissue-based RAS exacerbates
pulmonary hypertension, acute lung injury and experimental lung fibrosis [8]. Thus, blocking of
the Angiotensin II receptor type I (AT1R) was associated with reduced SARS-CoV spike protein
mediated lung injury [6] and reduced pulmonary hypertension in experimental models [9].
...
In supportive of the view that ACE2 expression prevents intestinal inflammation [11, 12], bioinformatic analysis suggested that genes regulating y tpe I and type III innate immunity, NK and T cell mediated cytotoxicity and energy metabolism are positively associated with ACE2 expression.
-------------------------------------------------------------
AT1R blocker effect=AT2R agonist
"""C21, a first in class low molecular weight angiotensin II receptor type 2 (AT2R) agonist, belongs to the “protective arm” of the renin angiotensin system (RAS), and is under development for idiopathic pulmonary fibrosis (IPF) and is also being studied in systemic sclerosis. Internal preclinical findings with C21 and the fact that the RAS plays a key role in the development of COVID-19 suggested that C21 could have a role in the treatment of the disease. This prompted Vicore Pharma to initiate a dialogue with the MHRA who invite initiatives to explore treatments for COVID-19.
There is a good scientific rationale for studying C21 as a potential treatment of COVID-19. It has recently been shown that the SARS CoV-2 virus utilizes the enzyme ACE2, which is part of RAS, for entry into the cell. This inactivates the ACE2 enzyme, creating an imbalance in the local RAS, leading to acute lung injury. Given that ACE2 generates the natural ligands for AT2R, Vicore Pharma believes that, by acting directly on the AT2R, C21 may suppress inflammatory mediators and bypass the way by which the virus incapacitates the system."""
Vicore Pharma submits Letter of Intent for a clinical trial application for a phase II study in patients with COVID-19, SARS CoV-2 infection | HealthCap
BUT it could be more difficult to fight pathogens without inflammation...
Bruna GG Pinto, Antonio ER Oliveira, Youvika Singh, Leandro Jimenez, Andre NA Goncalves, Rodrigo LT Ogava, Rachel Creighton, Jean PS Peron, View ORCID ProfileHelder I Nakaya
doi: ACE2 Expression is Increased in the Lungs of Patients with Comorbidities Associated with Severe COVID-19
This article is a preprint and has not been peer-reviewed [what does this mean?]. It reports new medical research that has yet to be evaluated and so should not be used to guide clinical practice.
Highly ACE2 Expression in Pancreas May Cause Pancreas Damage After SARS-CoV-2 Infection
Furong Liu, Xin Long, Wenbin Zou, Minghao Fang, Wenjuan Wu, Wei Li, Bixiang Zhang, Wanguang Zhang, Xiaoping Chen, Zhanguo Zhang
doi: Highly ACE2 Expression in Pancreas May Cause Pancreas Damage After SARS-CoV-2 Infection
This article is a preprint and has not been peer-reviewed [what does this mean?]. It reports new medical research that has yet to be evaluated and so should not be used to guide clinical practice.
"We found ACE2 was expressed in many
organs or tissues except most brain tissues (Fig. 1A), which suggests that these organs
or tissues such as unreported ovary and thyroid might also be targets for SARS-CoV-2."
ACE2 expression by colonic epithelial cells is associated with viral infection, immunity and energy metabolism
Jun Wang, Shanmeizi Zhao, Ming Liu, Zhiyao Zhao, Yiping Xu, Ping Wang, Meng Lin, Yanhui Xu, Bing Huang, Xiaoyu Zuo, Zhanghua Chen, Fan Bai, Jun Cui, Andrew M Lew, Jincun Zhao, Yan Zhang, Haibin Luo, Yuxia Zhang
doi: ACE2 expression by colonic epithelial cells is associated with viral infection, immunity and energy metabolism
This article is a preprint and has not been peer-reviewed [what does this mean?]. It reports new medical research that has yet to be evaluated and so should not be used to guide clinical practice.
Paradoxically, although ACE2 mediates viral entry to the host, its deficiency worsens lung injury
by activating the renin-angiotensin system (RAS) in experimental models [6]. The circulating
RAS regulates blood pressure and fluid homeostasis. Local tissue-based RAS exacerbates
pulmonary hypertension, acute lung injury and experimental lung fibrosis [8]. Thus, blocking of
the Angiotensin II receptor type I (AT1R) was associated with reduced SARS-CoV spike protein
mediated lung injury [6] and reduced pulmonary hypertension in experimental models [9].
...
In supportive of the view that ACE2 expression prevents intestinal inflammation [11, 12], bioinformatic analysis suggested that genes regulating y tpe I and type III innate immunity, NK and T cell mediated cytotoxicity and energy metabolism are positively associated with ACE2 expression.
-------------------------------------------------------------
AT1R blocker effect=AT2R agonist
"""C21, a first in class low molecular weight angiotensin II receptor type 2 (AT2R) agonist, belongs to the “protective arm” of the renin angiotensin system (RAS), and is under development for idiopathic pulmonary fibrosis (IPF) and is also being studied in systemic sclerosis. Internal preclinical findings with C21 and the fact that the RAS plays a key role in the development of COVID-19 suggested that C21 could have a role in the treatment of the disease. This prompted Vicore Pharma to initiate a dialogue with the MHRA who invite initiatives to explore treatments for COVID-19.
There is a good scientific rationale for studying C21 as a potential treatment of COVID-19. It has recently been shown that the SARS CoV-2 virus utilizes the enzyme ACE2, which is part of RAS, for entry into the cell. This inactivates the ACE2 enzyme, creating an imbalance in the local RAS, leading to acute lung injury. Given that ACE2 generates the natural ligands for AT2R, Vicore Pharma believes that, by acting directly on the AT2R, C21 may suppress inflammatory mediators and bypass the way by which the virus incapacitates the system."""
Vicore Pharma submits Letter of Intent for a clinical trial application for a phase II study in patients with COVID-19, SARS CoV-2 infection | HealthCap
BUT it could be more difficult to fight pathogens without inflammation...
Last edited:
md_a
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- Joined
- Aug 31, 2015
- Messages
- 468
Many readers of the Post must be taking angiotension receptor blockers (ARBs) for high blood pressure. As products these are tagged with names ending in “-sartan.” My personal poison is candesartan, but there’s a losartan, a valsartan and many others. We’ll call them “sartans” here to cut down on the acronyms.
In my column for Saturday’s paper I gave a whimsical overview of hypothetical treatments for COVID-19, and I forgot to so much as mention the sartans. Strange error for me to make. But it could be because these drugs have undergone a strange swing in reputation in the COVID era.
For a few weeks physicians and researchers studying COVID and the nasty little cuss that causes it, SARS-CoV-2, were nervous about the sartans (and their older cousins, the ACE inhibitors). It had quickly become apparent that SARS-CoV-2, like the classic SARS virus Canadians know too well, uses the natural enzyme ACE2 to penetrate cell walls in the lung and possibly other organs.
ACE2 is “angiotensin converting enzyme 2.” It is part of the fiendishly complicated “renin-angiotensin” hormone system that the kidney uses to tell the rest of the body to send it enough blood to do its job. This is the same system that the sartans fool with to lower your blood pressure, so there was an immediate question of interaction between the drug, the enzyme and the virus that exploits the enzyme.
Sartans increase ACE2 expression: they “upregulate” it, in the language of pharmacologists. This sounds bad if you’re frightened of a virus that uses ACE2 opportunistically to turn your lungs into hamburger. It sounded bad to enough family doctors that medical authorities had to put out advisories telling them not to run wild and start switching their high blood pressure patients away from sartans.
This now seems like a good call, because the latest thinking — subject to change at any moment, no doubt — is that sartans might actually help fend off the virus. Original SARS was shown in mice to actually “downregulate” or reduce ACE2 while exploiting it; this caused high blood pressure and lung failure, making the virus more or less the opposite of a sartan. Taking sartans actually appears to give you more ACE2 receptors, and that is, paradoxically, what you might want. Rather than increasing the attack surface for the virus, it gives you more receptors to spare so that the system keeps working.
Well, there are about two dozen people on Earth who understand this stuff and I’m not one of them. But the concept seems credible to those who studied original SARS closely. They even thought about using sartans as a treatment for SARS when there still seemed some danger it would run amuck, as SARS-2 is doing.
This is all theory (an “untested mechanistic hypothesis”, grumble the Olympian deities of evidence-based medicine), but it has found some empirical support. As the COVID virus was executing its cavalry charge through the city of Wuhan and Hubei province, a group of Chinese doctors were retrospectively studying the medication histories of persons who had both COVID and chronic high blood pressure. They wanted to check whether sartans and other pills for hypertension were bad. In their data, sartans came out looking very good, with users having significantly lower odds of developing severe COVID. It is an effect strong enough to have shown up in a fairly small universe of 511 patients.
I am not promising that the sartans will save us, but if you are a fellow user, you can feel slightly more comfortable about having to take 'em.
Colby Cosh on COVID-19: Sartans at Thermopylae? Blood pressure meds vs. the coronavirus
In my column for Saturday’s paper I gave a whimsical overview of hypothetical treatments for COVID-19, and I forgot to so much as mention the sartans. Strange error for me to make. But it could be because these drugs have undergone a strange swing in reputation in the COVID era.
For a few weeks physicians and researchers studying COVID and the nasty little cuss that causes it, SARS-CoV-2, were nervous about the sartans (and their older cousins, the ACE inhibitors). It had quickly become apparent that SARS-CoV-2, like the classic SARS virus Canadians know too well, uses the natural enzyme ACE2 to penetrate cell walls in the lung and possibly other organs.
ACE2 is “angiotensin converting enzyme 2.” It is part of the fiendishly complicated “renin-angiotensin” hormone system that the kidney uses to tell the rest of the body to send it enough blood to do its job. This is the same system that the sartans fool with to lower your blood pressure, so there was an immediate question of interaction between the drug, the enzyme and the virus that exploits the enzyme.
Sartans increase ACE2 expression: they “upregulate” it, in the language of pharmacologists. This sounds bad if you’re frightened of a virus that uses ACE2 opportunistically to turn your lungs into hamburger. It sounded bad to enough family doctors that medical authorities had to put out advisories telling them not to run wild and start switching their high blood pressure patients away from sartans.
This now seems like a good call, because the latest thinking — subject to change at any moment, no doubt — is that sartans might actually help fend off the virus. Original SARS was shown in mice to actually “downregulate” or reduce ACE2 while exploiting it; this caused high blood pressure and lung failure, making the virus more or less the opposite of a sartan. Taking sartans actually appears to give you more ACE2 receptors, and that is, paradoxically, what you might want. Rather than increasing the attack surface for the virus, it gives you more receptors to spare so that the system keeps working.
Well, there are about two dozen people on Earth who understand this stuff and I’m not one of them. But the concept seems credible to those who studied original SARS closely. They even thought about using sartans as a treatment for SARS when there still seemed some danger it would run amuck, as SARS-2 is doing.
This is all theory (an “untested mechanistic hypothesis”, grumble the Olympian deities of evidence-based medicine), but it has found some empirical support. As the COVID virus was executing its cavalry charge through the city of Wuhan and Hubei province, a group of Chinese doctors were retrospectively studying the medication histories of persons who had both COVID and chronic high blood pressure. They wanted to check whether sartans and other pills for hypertension were bad. In their data, sartans came out looking very good, with users having significantly lower odds of developing severe COVID. It is an effect strong enough to have shown up in a fairly small universe of 511 patients.
I am not promising that the sartans will save us, but if you are a fellow user, you can feel slightly more comfortable about having to take 'em.
Colby Cosh on COVID-19: Sartans at Thermopylae? Blood pressure meds vs. the coronavirus
S.Seneff
Member
- Joined
- Mar 18, 2020
- Messages
- 215
Among COVID-19 patients with hypertension, those received either ARBs/ACEIs or non-ARBs/ACEIs had comparable blood pressure. However, ARBs/ACEIs group had significantly lower concentrations of CRP (p=0.049) and procalcitonin (PCT, p=0.008). Furthermore, much lower proportion of critical patients (9.3% vs 22.9%; p=0.061), and a lower death rate (4.7% vs 13.3%; p=0.216) were observed in ARBs/ACEIs group than non-ARBs/ACEIs group, although these differences failed to reach statistical significance. Our findings thus support the use of ARBs/ACEIs in COVID-19 patients with preexisting hypertension.
Guang Yang, Zihu Tan, Ling Zhou, Min Yang, Lang Peng, Jinjin Liu, Jingling Cai, Ru Yang, Junyan Han, Yafei Huang, Shaobin He
doi: https://doi.org/10.1101/2020.03.31.20038935
GenericName86
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- Jun 30, 2018
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- 338
So at the moment would it be wise to ease off anything that's supplemental that may increase ACE2?
JohnHafterson
Member
I like this schematic of Renin Angiotensin System. Well laid out. RAS seems like it has redundant/alternate ways to limit negative downstreams, ACEIs and ARBs benefit at different points.
Beneficials in order of importance:
#1 AT1 receptor downregulation, blocking, or limitation
#2 Ang 1-7 (masr "mas receptor)
#3 AT2 receptor agonsim
freedom
Member
- Joined
- Dec 19, 2014
- Messages
- 19
Great schematic of Renin Angiotensin System clearly demonstrating the importance of ACE2/ACE ratio. Ray has mentioned how the binding of ACE2 with COVID-19 virus could lead to high levels of ANG2 and then AT1R(bad).
The following study shows how moderate intensity continuous exercise (MICE) decreases ACE(good) while high intensity interval exercise (HIIE) increases ACE2(good):
Two protocols of aerobic exercise modulate the counter-regulatory axis of the renin-angiotensin system
3.1. Plasma levels of RAS components
The MICE protocol resulted in a decrease in plasma levels of ACE [(Figure 2 A; p < 0.05 Bonferroni post-test). Two-way ANOVA results for plasma ACE = Exercise protocol: F(1,18) = 0.00, p = 0.9961; Time: F(1,18) = 1.00, p = 0.3299; Exercise Protocol x Time: F(1,18) = 7.76, p =2. On the 0.012other hand, the HIIE protocol resulted in a significant increase in ACE2 levels
The following study shows how moderate intensity continuous exercise (MICE) decreases ACE(good) while high intensity interval exercise (HIIE) increases ACE2(good):
Two protocols of aerobic exercise modulate the counter-regulatory axis of the renin-angiotensin system
3.1. Plasma levels of RAS components
The MICE protocol resulted in a decrease in plasma levels of ACE [(Figure 2 A; p < 0.05 Bonferroni post-test). Two-way ANOVA results for plasma ACE = Exercise protocol: F(1,18) = 0.00, p = 0.9961; Time: F(1,18) = 1.00, p = 0.3299; Exercise Protocol x Time: F(1,18) = 7.76, p =2. On the 0.012other hand, the HIIE protocol resulted in a significant increase in ACE2 levels
S.Seneff
Member
- Joined
- Mar 18, 2020
- Messages
- 215
Reduced expression of COVID-19 host receptor, ACE2 is associated with small bowel inflammation, more severe disease, and response to anti-TNF therapy in Crohn′s disease
View ORCID ProfileAlka A Potdar, Shishir Dube, Takeo Naito, Gregory Botwin, View ORCID ProfileTalin Haritunians, Dalin Li, Shaohong Yang, View ORCID ProfileJanine Bilsborough, Lee A Denson, Mark Daly, Stephan R Targan, Phillip Fleshner, Jonathan Braun, Subra Kugathasan, Thaddeus S Stappenbeck, Dermot P B McGovern
doi: https://doi.org/10.1101/2020.04.19.20070995
This article is a preprint and has not been certified by peer review [what does this mean?]. It reports new medical research that has yet to be evaluated and so should not be used to guide clinical practice.
Cluster of COVID-19 in northern France: A retrospective closed cohort study
Arnaud Fontanet, Laura Tondeur, View ORCID ProfileYoann Madec, View ORCID ProfileRebecca Grant, Camille Besombes, Nathalie Jolly, Sandrine Fernandes Pellerin, Marie-Noelle Ungeheuer, Isabelle Cailleau, Lucie Kuhmel, Sarah Temmam, Christele Huon, Kuang-Yu Chen, Bernadette Crescenzo, Sandie Munier, Caroline Demeret, Ludivine Grzelak, Isabelle Staropoli, Timothee Bruel, Pierre Gallian, Simon Cauchemez, Sylvie van der Werf, Olivier Schwartz, Marc Eloit, Bruno Hoen
doi: https://doi.org/10.1101/2020.04.18.20071134
This article is a preprint and has not been certified by peer review [what does this mean?]. It reports new medical research that has yet to be evaluated and so should not be used to guide clinical practice.
Abstract
Background: The Oise department in France has been heavily affected by COVID-19 in early 2020. Methods: Between 30 March and 4 April 2020, we conducted a retrospective closed cohort study among pupils, their parents and siblings, as well as teachers and non-teaching staff of a high-school located in Oise. Participants completed a questionnaire that covered history of fever and/or respiratory symptoms since 13 January 2020 and had blood tested for the presence of anti-SARS-CoV-2 antibodies. The infection attack rate (IAR) was defined as the proportion of participants with confirmed SARS-CoV-2 infection based on antibody detection. Blood samples from two blood donor centres collected between 23 and 27 March 2020 in the Oise department were also tested for presence of anti-SARS-CoV-2 antibodies. Findings: Of the 661 participants (median age: 37 years), 171 participants had anti-SARS-CoV-2 antibodies. The overall IAR was 25.9% (95% confidence interval (CI) = 22.6-29.4), and the infection fatality rate was 0% (one-sided 97.5% CI = 0-2.1). Nine of the ten participants hospitalised since mid-January were in the infected group, giving a hospitalisation rate of 5.3% (95% CI = 2.4-9.8). Anosmia and ageusia had high positive predictive values for SARS-CoV-2 infection (84.7% and 88.1%, respectively). Smokers had a lower IAR compared to non-smokers (7.2% versus 28.0%, P <0.001). The proportion of infected individuals who had no symptoms during the study period was 17.0% (95% CI = 11.2-23.4). The proportion of donors with anti-SARS-CoV-2 antibodies in two nearby blood banks of the Oise department was 3.0% (95% CI = 1.1-6.4). Interpretation: The relatively low IAR observed in an area where SARS-CoV-2 actively circulated weeks before confinement measures indicates that establishing herd immunity will take time, and that lifting these measures in France will be long and complex.
View ORCID ProfileAlka A Potdar, Shishir Dube, Takeo Naito, Gregory Botwin, View ORCID ProfileTalin Haritunians, Dalin Li, Shaohong Yang, View ORCID ProfileJanine Bilsborough, Lee A Denson, Mark Daly, Stephan R Targan, Phillip Fleshner, Jonathan Braun, Subra Kugathasan, Thaddeus S Stappenbeck, Dermot P B McGovern
doi: https://doi.org/10.1101/2020.04.19.20070995
This article is a preprint and has not been certified by peer review [what does this mean?]. It reports new medical research that has yet to be evaluated and so should not be used to guide clinical practice.
- Abstract
Cluster of COVID-19 in northern France: A retrospective closed cohort study
Arnaud Fontanet, Laura Tondeur, View ORCID ProfileYoann Madec, View ORCID ProfileRebecca Grant, Camille Besombes, Nathalie Jolly, Sandrine Fernandes Pellerin, Marie-Noelle Ungeheuer, Isabelle Cailleau, Lucie Kuhmel, Sarah Temmam, Christele Huon, Kuang-Yu Chen, Bernadette Crescenzo, Sandie Munier, Caroline Demeret, Ludivine Grzelak, Isabelle Staropoli, Timothee Bruel, Pierre Gallian, Simon Cauchemez, Sylvie van der Werf, Olivier Schwartz, Marc Eloit, Bruno Hoen
doi: https://doi.org/10.1101/2020.04.18.20071134
This article is a preprint and has not been certified by peer review [what does this mean?]. It reports new medical research that has yet to be evaluated and so should not be used to guide clinical practice.
Abstract
Background: The Oise department in France has been heavily affected by COVID-19 in early 2020. Methods: Between 30 March and 4 April 2020, we conducted a retrospective closed cohort study among pupils, their parents and siblings, as well as teachers and non-teaching staff of a high-school located in Oise. Participants completed a questionnaire that covered history of fever and/or respiratory symptoms since 13 January 2020 and had blood tested for the presence of anti-SARS-CoV-2 antibodies. The infection attack rate (IAR) was defined as the proportion of participants with confirmed SARS-CoV-2 infection based on antibody detection. Blood samples from two blood donor centres collected between 23 and 27 March 2020 in the Oise department were also tested for presence of anti-SARS-CoV-2 antibodies. Findings: Of the 661 participants (median age: 37 years), 171 participants had anti-SARS-CoV-2 antibodies. The overall IAR was 25.9% (95% confidence interval (CI) = 22.6-29.4), and the infection fatality rate was 0% (one-sided 97.5% CI = 0-2.1). Nine of the ten participants hospitalised since mid-January were in the infected group, giving a hospitalisation rate of 5.3% (95% CI = 2.4-9.8). Anosmia and ageusia had high positive predictive values for SARS-CoV-2 infection (84.7% and 88.1%, respectively). Smokers had a lower IAR compared to non-smokers (7.2% versus 28.0%, P <0.001). The proportion of infected individuals who had no symptoms during the study period was 17.0% (95% CI = 11.2-23.4). The proportion of donors with anti-SARS-CoV-2 antibodies in two nearby blood banks of the Oise department was 3.0% (95% CI = 1.1-6.4). Interpretation: The relatively low IAR observed in an area where SARS-CoV-2 actively circulated weeks before confinement measures indicates that establishing herd immunity will take time, and that lifting these measures in France will be long and complex.
JohnHafterson
Member
Probably beneficial due to effect of shift from glycolysis to aerobic metabolism.
Anything which effects energy effects inflammation, immunity, etc.
I would just take Thiamine B1 instead of DCA. A view of B1 on HIV, B1 has favorable impact on RAAS.
I don't think you need to take anything "sexy" for Covid19. Basic things all impact RAAS.
Vitamin D
Vitamin D alleviates lipopolysaccharide‑induced acute lung injury via regulation of the renin‑angiotensin system
Vitamin E
Antioxidants Block Angiotensin II-Induced Increases in Blood Pressure and Endothelin
Vitamin C
Ascorbic Acid Decreases the Binding Affinity of the AT1 Receptor for Angiotensin II
Magnesium
Magnesium Supplementation Prevents Angiotensin II-induced Myocardial Damage and CTGF Overexpression
Taurine
Interaction between the actions of taurine and angiotensin II
Ginger - a natural ARB "artan"
[6]-gingerol: A Novel AT1 Antagonist for the Treatment of Cardiovascular Disease
EMF Mitigation - Flush Niacin - Big 5 Minerals
