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How does one defeat the COVID-19 virus? This is one question that has been plaguing the minds of scientists since the virus emerged in 2019. Little did one know then that it would go on to trigger a pandemic that claimed millions of lives and was seemingly invincible. Today, we have many vaccines, which can work against the virus and a few repurposed drugs. But then, the emergence of mutated strains, variants of concern, have negated the efficacy of these drugs and vaccines to a certain extent. To overcome these setbacks, researchers played with the theory of using the COVID-19 virus against itself. The end result of this is that scientists have come up with a design of a new COVID-19 therapy, which uses a defective version of the SARS-CoV-2 virus to drive the disease-causing version to extinction. The journal PeerJ published this study.
Researchers from Penn State have now designed a synthetic defective SARS-CoV-2 virus that is harmless. But it can interfere with the growth of the disease-causing virus. This, say researchers, can lead to the extinction of both the disease-causing virus and the synthetic virus. During the course of their study, they saw that the disease-causing COVID-19 virus actually induces the replication and spread of their synthetic virus and promotes its own decline. They are optimistic that a version of this synthetic virus can be used as a self-promoting antiviral therapy for COVID-19.
When a virus attacks a cell, it attaches itself to the cell's surface and injects its genetic material into it. This tricks the cell into replicating the virus's genetic material. It then takes on the form of virions, which travel from the cell and go on to infect other cells. Now, we have defective interfering (DI) viruses, with large deletions in their genomes, which affect their ability to replicate their genetic material and package it into virions. But, DI genomes can perform these functions if the cell they've infected also contains genetic material from a wild-type virus. They do this by hijacking a wild-type genome's replication and packaging machinery.
These defective genomes are like parasites of the wild-type virus. When a DI genome utilizes of a wild-type genome's machinery, it can impair the wild-type genome growth. Moreover, because of the shorter length of their genomes as a result of the deletions, DI genomes can replicate faster than wild-type genomes in coinfected cells and quickly outcompete the wild-type.
According to the researchers, their synthetic DI genome can replicate three times faster than the wild-type genome. This results in a reduction of the wild-type viral load by half in 24 hours. However, they caution that the 50 per cent reduction in virus load that they observed over 24 hours is not enough for therapeutic purposes. This is because as the DI genomes increase in frequency in the cell, the decline in the amount of wild-type virus would lead to the death of both the virus and the DI genome, as the DI genome cannot persist once it has driven the wild-type virus to extinction. But they are hopeful that further experiments may be able to verify the potential of SARS-CoV-2 DIs as an antiviral treatment, provided an efficient delivery method is devised. It could indeed become a self-sustaining therapeutic for COVID-19, they say.
(With inputs from Agencies)
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