Researchers at Penn State are Turning COVID-19 on Itself

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Researchers at Penn State are Turning COVID-19 on Itself Using a defective version of the SARS-CoV-2 virus, researchers at Penn State hope to drive the disease-causing version to extinction. The team designed a synthetic defective virus that interferes with the real virus, potentially able to cause the extinction of both the disease-causing virus and the synthetic defective. The researchers observed that the disease-causing virus "actually enables the replication and spread of [the] synthetic virus", according to Marco Archetti, associate professor of biology at Penn State. He also notes that a new version of this synthetic construct could be used as a "self-promoting antiviral therapy for COVID-19". How does the therapy work? In order to understand this, it's important to understand how viruses work. When a virus attacks a cell, it attaches to the surface of the cell and injects its genetic material into the cell. The cell is tricked into replicating the virus until it bursts, sending the new viruses off to infect other cells. "Defective interfering" viruses, or DI viruses, which are common in nature, contain deletions in their genomes which can make them unable to attack cells. However, with the help of COVID-19, or wild-type viruses, these DI viruses are able to replicate. In other words, the DI genome can hijack a wild-type genome's replication machinery. These defective genomes work like "parasites of the wild-type virus", said Archetti, explaining that DI genomes use the wild-type genomes machinery to impair its growth. Additionally, DI genomes can replicate faster than wild-type genomes and outcompete the wild-type. In fact, their new study, published in the journal PeerJ, found that the DI genome can replicate three times faster than the wild-type genome, resulting in a lower wild-type viral load by half in one day. The study was done by engineering short synthetic DI genomes from the wild-type SARS-CoV-2 genome and introducing them to African green monkey cells already infected with the wild-type virus. The scientists then measured the relative amounts of DI and wild-type viruses, giving an indication of the interference. Though according to Archetti, the 50% reduction in virus load that they observed over 24 hours is not enough for any therapeutic purposes, presumably the DI genomes could increase in frequency and eventually lead to both the demise of the virus and the DI genome, because the DI cannot persist without the wild-type virus. Archetti says that with "some additional research and fine-tuning", this synthetic DI could be used as a "self-sustaining therapeutic for COVID-19". Reference: “A synthetic defective interfering SARS-CoV-2” by Shun Yao, Anoop Narayanan, Sydney A. Majowicz, Joyce Jose​ Marco Archetti​, 1 July 2021, PeerJ.

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