A study, published in Nature, looked at a large-scale screen of potential anti-SARS-CoV-2 drugs.
Dr Stephen Griffin, Associate Professor in the School of Medicine, University of Leeds, said:
“As the SARS-CoV2 pandemic continues to afflict much of the planet, it is clear that having as many weapons in our arsenal to combat this virus is of paramount importance. Whilst we know from extensive trials that remdesivir is able to reduce virus replication and improve clinical outcomes, and dexamethasone can alleviate some of the severe immunological consequences of severe COVID19, the availability of additional lines of therapy could be critical in controlling the sometimes severe, and often long term clinical sequelae of SARS-CoV2 infection. Moreover, such therapies will need to be widely available across the globe, including lower and middle income countries, so the idea of repurposing generic and/or approved drugs should be greatly enabling in this regard. However, going forward it will also be desirable to develop bespoke SARS-CoV2 therapies to mitigate the possible emergence of virus resistance.
“This study is on an impressive scale and has been well conducted, identifying numerous compounds with measurable potency. The majority appear targeted against virus-host interactions, with proteases and also the PIKFYVE pathway being prominent, as seen in other investigations. This convergence of targets is encouraging and clearly points to potential Achilles heels that might be exploited in the future. As shown for remdesivir, such drugs could also theoretically be used in conjunction with direct-acting antivirals for more effective therapies.”
Prof Ian Jones, Professor of Virology, University of Reading, said:
“This study is a tour de force of the ability to rapidly screen existing drugs for their ability to inhibit SARS-CoV-2. The advantage of this approach is that the drugs are already in use for other conditions so could be repurposed immediately for use in Covid cases. The disadvantage of any of these drugs however is that they need to be given as early as possible in order to stop the damage done by the virus but, as mild symptoms are common, at least in early infection, any therapies used are not initiated until an individual is hospitalised, which is a bit late. Attacking the virus itself once lung damage or thrombosis is triggered may not be very effective, as has been the case in many of the trials to date. The ideal situation would be widespread testing followed by a “flu friend” like system of drug distribution as soon as a positive is identified. That would lower the number of people getting seriously ill as well as reducing virus numbers and so transmissibility.”
‘Discovery of SARS-CoV-2 antiviral drugs through large-scale compound repurposing’ by Riva et al was published in Nature on Friday 24th July 2020.
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Prof Ian Jones: None
Dr Stephen Griffin: No conflicts