Researchers Find a Drug That Can Inhibit COVID-19 Virus Replication By Up to 5000 Fold

Every few years, a new virus outbreak occurs that affects thousands of people such as the SARS-CoV in 2003, Ebola in 2014, and now the SARS-CoV-2 since December 2019. These frequent outbreaks have proved to be specially challenging as treatment discoveries have a time constraint.

Coronavirus

Coronavirus

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SARS-CoV-2 results in COVID-19, that has flu like symptoms ranging from mild disease to severe lung injury and multi-organ failure, eventually leading to death, especially in older patients with other co-morbidities. Since the WHO declaration of COVID-19 to be a public health emergency of pandemic proportions, researchers around the world have been racing against time to find an effective treatment.

University of British Columbia published results of a clinical trial recently that have promising findings of a potentially effective drug. According to the researchers, hrsACE2, which has already been tested in phase 1 and phase 2 clinical trials, can reduce viral growth by a factor of 1,000-5,000.

The study found the receptor binding domain (RBD) of SARS-CoV-2 to be remarkably similar to the SARS-CoV RBD, signifying a similar host cell receptor. Additionally, the researchers found ACE2 to be the functional SARS-CoV receptor by in vitro study.

A study conducted on mice found overexpression of ACE2 to enhance severity of disease in mice infected with SARS-CoV. This indicates that ACE2-dependent viral entry into cells is a critical factor for morbidity. Injecting SARS-CoV spike into mice decreased ACE2 expression levels, thereby worsening lung injury.

Recent studies have shown that SARS-CoV-2 spike protein directly binds to ACE2 and that the SARS-CoV-2 spike protein recognizes human ACE2 with even higher binding affinity than Spike from SARS-CoV.

In human lung, ACE2 is found mainly in alveolar epithelial type II cells, which can also acts as a viral storage. These cells synthesize surfactant which lessens surface tension inhibiting alveolar collapse. Therefore, they are essential to the lung’s gas exchange function. In COVID-19, the severity of illness can be attributed to the damage of the alveolar epithelial type II cells, that express ACE2.

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Apart from the lungs, ACE2 is also expressed in the heart, kidneys, blood vessels, and intestine. This explains the multiorgan dysfunction seen in COVID-19 patients.

According to the researchers, clinical-grade human recombinant soluble ACE2 can reduce viral growth in COVID-19 infected cells by a factor of 1,000-5,000. The drug has already been tested in phase 1 and phase 2 clinical trials. Furthermore, hrsACE2 can inhibit the infection of human blood vessels and kidney even at the early stages of infection.

The researchers aimed to provide direct evidence that clinical-grade hrsACE2 can indeed interfere with SARS-CoV-2 infections. At first they infected cells with varying numbers of SARS-CoV-2. Next using qRT-PCR, Viral RNA was purified from cells and assayed to use it as a marker for replication.

Infection of cells in the presence of hrsACE2 during 1 hr, followed by washing and incubation without hrsACE2 significantly inhibited SARS-CoV-2 infections 15 hours post infection.

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The team led by University of British Columbia researcher Dr. Josef Penninger have found hrsACE2 to effectively block the receptor SARS-CoV-2 uses to infect its hosts.

“Our new study provides very much needed direct evidence that a drug — called APN01 (human recombinant soluble angiotensin-converting enzyme 2 — hrsACE2) — soon to be tested in clinical trials by the European biotech company Apeiron Biologics, is useful as an antiviral therapy for COVID-19,” says Dr. Art Slutsky, a scientist at the Keenan Research Centre for Biomedical Science of St. Michael’s Hospital and professor at the University of Toronto who is a collaborator on the study.

Emergency funding to combat the COVID-19 outbreak from the Canadian federal government has supported part of the research.

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Reference:

https://www.cell.com/pb-assets/products/coronavirus/CELL_CELL-D-20-00739.pdf

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