I first read of this hypothesized link on this site here where such a link is discussed in various articles:

Recently, here at FBEL, there was a presentation of the very plausible theory that “Covid-19”, in what we might start to call its truest sense, is caused by coronavirus interacting with Angiotensin-Converting Enzyme 2 (ACE2) receptors expressed in the lungs. It was further posited that a prevalence of ACE2 was a side effect of treatment with ACE inhibitors (ACEI), and angiotensin receptor blockers (ARBs) for hypertension.

Now we look at further evidence that reinforces the fact of the manner of lung infection proposed in the theory, and how ACEIs and ARBs appear to be being used expressly to promote ACE2s for what is limitedly understood to be medicinal qualities; in other words, the ACE2s are not intended to be side effects, but a factor in the treatment. As such, an environment for a limited amount of success by a coronavirus that attacks the lungs has been... [in essence] created by the medical establishment.

This article on another site examines the issue further and in a readable manner.

What is the ACE2 receptor, how is it connected to coronavirus and why might it be key to treating COVID-19?

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In the search for treatments for COVID-19, many researchers are focusing their attention on a specific protein that allows the virus to infect human cells. Called the angiotensin-converting enzyme 2, or ACE2 “receptor,” the protein provides the entry point for the coronavirus to hook into and infect a wide range of human cells. Might this be central in how to treat this disease? 

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What are ACE inhibitors? Are they a possible treatment or prophylactic for SARS-CoV-2?

 

Angiotensin converting enzyme (ACE, aka ACE1) is another protein, also found in tissues such as the lung and heart, where ACE2 is present. Drugs that inhibit the actions of ACE1 are called ACE inhibitors. Examples of these drugs are ramipril, lisinopril, and enalapril. These drugs block the actions of ACE1 but not ACE2. ACE1 drives the production of ANG II. In effect, ACE1 and ACE2 have a “yin-yang” relationship; ACE1 increases the amount of ANG II, whereas ACE2 reduces ANG II.

 

By inhibiting ACE1, ACE inhibitors reduce the levels of ANG II and its ability to increase blood pressure and tissue injury. ACE inhibitors are commonly prescribed for patients with hypertension, heart failure and kidney disease.

 

Another commonly prescribed class of drugs, angiotensin receptor blockers (ARBs, e.g., losartan, valsartan, etc.) have similar effects to ACE inhibitors and may also be useful in treating COVID-19.

 

Evidence for a protective effect of ACE inhibitors and angiotensin receptor blockers in patients with COVID-19 was shown in recent work co-authored by one of us - Dr. Loomba.

No evidence exists to suggest prophylactic use of these drugs; we do not advise readers to take these drugs in the hopes that they will prevent COVID-19. We wish to emphasize that patients should only take these drugs as instructed by their health care provider.

 

New clinical trial tests ACE inhibitor against SARS-CoV-2: In collaboration with a multidisciplinary group of investigators, Dr. Loomba has initiated a multicenter (randomized, double-blinded, placebo-controlled) clinical trial to examine the efficacy of ramipril - an ACE inhibitor - compared to a placebo in reducing mortality, ICU admission or need for mechanical ventilation in patients with COVID-19.

However, maybe unfortunately, recently published studies do not indicate that ACE inhibitors are useful in respect of lowing CV19 risk or outcome (though this can be considered good news in the sense that meds for diabetes, high blood pressure and/or obesity which raise ACE2 expression do not appear to raise the risk of contracting CV19 for an individual).

Some recent studies and their abstracts:

Good or bad: Application of RAAS inhibitors in COVID-19 patients with cardiovascular comorbidities

The coronavirus disease 2019 (COVID-19) pandemic is caused by a newly emerged coronavirus (CoV) called Severe Acute Respiratory Syndrome coronavirus 2 (SARS-CoV-2). COVID-19 patients with cardiovascular disease (CVD) comorbidities have significantly increased morbidity and mortality. The use of angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor type 1 blockers (ARBs) improve CVD outcomes; however, there is concern that they may worsen the prognosis of CVD patients that become infected with SARS-CoV-2 because the virus uses the ACE2 receptor to bind to and subsequently infect host cells. Thus, some health care providers and media sources have questioned the continued use of ACE inhibitors and ARBs. In this brief review, we discuss the effect of ACE inhibitor-induced bradykinin on the cardiovascular system, on the renin–angiotensin–aldosterone system (RAAS) regulation in COVID-19 patients, and analyze recent clinical studies regarding patients treated with RAAS inhibitors. We propose that the application of RAAS inhibitors for COVID-19 patients with CVDs may be beneficial rather than harmful.

The interaction of RAAS inhibitors with COVID-19: Current progress, perspective and future

Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is currently defined as the worst pandemic disease. SARS-CoV-2 infects human cells via the binding of its S protein to the receptor angiotensin-converting enzyme (ACE2). The use of ACEIs/ARBs (RAAS inhibitors) regulates the renin-angiotensin-aldosterone system (RAAS) and may increase ACE2 expression. Considering the large use of ACEIs/ARBs in hypertensive patients, some professional groups are concerned about whether the use of RAAS inhibitors affects the risk of SARS-CoV-2 infection or the risk of severe illness and mortality in COVID-19 patients. In this review, we summarize preclinical and clinical studies to investigate whether the use of ACEIs/ARBs increases ACE2 expression in animals or patients. We also analyzed whether the use of these drugs affects the risk of SARS-CoV-2 infection, severe illness or mortality based on recent studies. Finally, the review suggests that current evidence does not support the concerns.

RAAS inhibitors do not increase the risk of COVID-19

According to five new studies, therapy with angiotensin-converting enzyme (ACE) inhibitors or angiotensin-receptor blockers (ARBs) is not associated with an increased risk of infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) or with an increased risk of severe disease or in-hospital death among patients with COVID-19.