Investigators at Cedars-Sinai have identified a potential new therapy for COVID-19: a biologic substance created by reengineered human skin cells.
In the study—co-funded by the California Institute for Regenerative Medicine (CIRM)—scientists found the substance stopped SARS-CoV-2, the virus that causes COVID-19, from reproducing itself. The substance also protected infected cells when tested in human lung cells.
Although still in the early stages, the findings open the possibility of having a new therapy for COVID-19 patients, of which there are few. Current COVID-19 treatments primarily focus on preventing the virus from replicating. This new potential treatment inhibits replication but also protects or repairs tissue, which is important because COVID-19 can cause symptoms that affect patients long after the viral infection has been cleared.
The potential therapy investigated in this study was created by scientists using skin cells called dermal fibroblasts. The investigators engineered the cells to produce therapeutic extracellular vesicles (EVs), which are nanoparticles that serve as a communication system between cells and tissue. Engineering these fibroblasts allowed them to secrete EVs—which the investigators dubbed “ASTEX”—with the ability to repair tissue.
The study tested ASTEX by applying it to human lung epithelial cells, cells that line the pulmonary tract and are the targets of SARS-CoV-2 infection. They discovered that ASTEX prevented cells from launching an inflammatory process that could lead to cell death. Cells treated with ASTEX also made fewer of a type of protein called ACE that SARS-CoV-2 may use to infect cells.
The team compared the new potential treatment with remdesivir, a drug currently used to treat COVID-19, and found that remdesivir did not inhibit production of ACE. Instead, remdesivir stops the virus from latching on to a protein called ACE2. ASTEX, therefore, may present another way to prevent the virus from entering cells.
“We were surprised to find this potential therapy shuts down a novel pathway for viral replication and also protects infected cells,” said Ahmed G. Ibrahim, PhD, MPH, assistant professor in the Smidt Heart Institute at Cedars-Sinai and first author of the study.
Investigators at Cedars-Sinai are planning future studies.