[GoodGrief]

Thank you all for this wonderful discussion. Repeating Cardcrimson's question, can anyone explain what the excerpt at the bottom means?

My 86 year-old mother currently takes Losartan (an ARB, which is also cited along with ACE Inhibitors as possibly being linked to severe Covid-19). She also takes Carvedilol (beta blocker) and Amlodipine Besylate (calcium blocker), as well as Metformin and Simvastain. Does anybody have an opinion if we should ask her doctor if she should stop taking the Losartan for now?

This article (https://www.bmj.com/content/368/bmj.m810/rr-2) suggests that ACE inhibitors taken for blood pressure control may play a role in the high Covid-19 mortality for older people and people with cardiovascular disease.  I've seen this speculation elsewhere, and it's interesting enough that someone needs to be looking into this.

Is a link between these observations possible? Is the expression of ACE2 receptor in the virus targeted cells increased by the use of ACE-inhibitor/angiotensin-receptor blocker and is the patient therefore more at risk for a severe course? We need rapid epidemiological and preclinical studies to clarify this relationship. If this were the case, we might be able to reduce the risk of fatal Covid-19 courses in many patients by temporarily replacing these drugs

Can one of the doctors out there please translate for those of us on these drugs. . . .

"On the one hand, it has been shown that the Covid-19 agent (also known as SARS-CoV-2), uses the SARS-COV receptor angiotensin converting enzyme (ACE) 2 for entry into target cells [4]. The interface between ACE2 and the viral spike protein SARS-S has been elucidated and the efficiency of ACE2 usage was found to be a key determinant of SARS-CoV transmissibility [4]. 

On the other hand, it could be shown in animal experiments that both the ACE-inhibitor lisinopril and the angiotensin-receptor blocker losartan can significantly increase mRNA expression of cardiac ACE2 (5-fold and 3-fold, respectively) [5]. Further, losartan also significantly increases cardiac ACE2 activity [5].
Is a link between these observations possible? Is the expression of ACE2 receptor in the virus targeted cells increased by the use of ACE-inhibitor/angiotensin-receptor blocker and is the patient therefore more at risk for a severe course? We need rapid epidemiological and preclinical studies to clarify this relationship. If this were the case, we might be able to reduce the risk of fatal Covid-19 courses in many patients by temporarily replacing these drugs."

[GoodGrief]

Thank you all for this wonderful discussion. Repeating Cardcrimson's question, can anyone explain what the excerpt at the bottom means?

My 86 year-old mother currently takes Losartan (an ARB, which is also cited along with ACE Inhibitors as possibly being linked to severe Covid-19). She also takes Carvedilol (beta blocker) and Amlodipine Besylate (calcium blocker), as well as Metformin and Simvastain. Does anybody have an opinion if we should ask her doctor if she should stop taking the Losartan for now?

This article (https://www.bmj.com/content/368/bmj.m810/rr-2) suggests that ACE inhibitors taken for blood pressure control may play a role in the high Covid-19 mortality for older people and people with cardiovascular disease.  I've seen this speculation elsewhere, and it's interesting enough that someone needs to be looking into this.

Is a link between these observations possible? Is the expression of ACE2 receptor in the virus targeted cells increased by the use of ACE-inhibitor/angiotensin-receptor blocker and is the patient therefore more at risk for a severe course? We need rapid epidemiological and preclinical studies to clarify this relationship. If this were the case, we might be able to reduce the risk of fatal Covid-19 courses in many patients by temporarily replacing these drugs

Can one of the doctors out there please translate for those of us on these drugs. . . .

"On the one hand, it has been shown that the Covid-19 agent (also known as SARS-CoV-2), uses the SARS-COV receptor angiotensin converting enzyme (ACE) 2 for entry into target cells [4]. The interface between ACE2 and the viral spike protein SARS-S has been elucidated and the efficiency of ACE2 usage was found to be a key determinant of SARS-CoV transmissibility [4]. 

On the other hand, it could be shown in animal experiments that both the ACE-inhibitor lisinopril and the angiotensin-receptor blocker losartan can significantly increase mRNA expression of cardiac ACE2 (5-fold and 3-fold, respectively) [5]. Further, losartan also significantly increases cardiac ACE2 activity [5].
Is a link between these observations possible? Is the expression of ACE2 receptor in the virus targeted cells increased by the use of ACE-inhibitor/angiotensin-receptor blocker and is the patient therefore more at risk for a severe course? We need rapid epidemiological and preclinical studies to clarify this relationship. If this were the case, we might be able to reduce the risk of fatal Covid-19 courses in many patients by temporarily replacing these drugs."