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PRESS RELEASE
5 December 2023
Dose matters: HIV drug could prevent coronaviruses, study finds
Coronaviruses are a global public health risk, with three highly infectious species, including SARS-CoV-2, emerging in the last 20 years. New research by the University of Bristol has shown how an HIV drug could stop many coronavirus diseases, including the SARS-CoV-2 variants, when given to infected cells at the right concentration. The findings could strengthen the arsenal of antiviral drugs available to combat current and future coronavirus outbreaks.
Currently, there are limited antiviral therapies available against SARS-CoV-2 - the virus that causes COVID-19, and these drugs are not always effective, highlighting the need for more treatments. Also, the virus can mutate, and its variants can become partially or completely resistant to some of the available treatments, such as monoclonal antibodies.
The research team has previously shown that a booster drug (cobicistat), which is normally used to reinforce the effect of anti-HIV drugs, could have antiviral properties against a SARS-CoV-2 variant circulating in Europe in early 2020.
In this study, published in Antiviral Research today [5 December] the researchers studied whether the anti-SARS-CoV-2 properties of cobicistat were maintained against the key variants of concern (VOCs) of SARS-CoV-2 and other coronaviruses, including Middle East respiratory syndrome coronavirus (MERS-CoV). MERS-CoV circulates in the Middle East, Africa and South Asia and has a death rate of over 30% with no vaccine or specific treatments being currently available. The team also compared the effects of cobicistat to those of ritonavir, which is a structurally similar molecule and also one of the components of Paxlovid, which is the current gold standard for antiviral treatment of SARS-CoV-2.
The research, using automated image analysis for a screening and parallel comparison of the anti-coronavirus effects of cobicistat and ritonavir, found cobicistat and ritonavir both act against all eight VOCs of SARS-CoV-2 that were tested as well as against other human coronaviruses, including MERS-CoV.
The findings indicate that cobicistat is more powerful than ritonavir. Both drugs displayed anti-coronavirus activity in vitro at dosages that are well tolerated, but higher than those currently used for booster activity of anti-HIV drugs and in Paxlovid. When used at these higher dosages cobicistat and ritonavir both inhibited coronavirus replication on their own and when combined with other drugs.
Dr Iart Luca Shytaj, Lecturer in the School of Cellular and Molecular Medicine and one of the paper’s corresponding authors, said: “Our results indicate that cobicistat, at dosages above its typical clinical use as a booster, could become an effective antiviral drug both on its own and in combination with other antivirals and lead to more potent treatments than current available options.
“If our findings are confirmed in animal and clinical studies, our results could strengthen the arsenal of antiviral drugs in the fight against current and future outbreaks of coronaviruses and reduce their impact on public health globally.”
Next steps for the research include animal and clinical testing of high-dose cobicistat in combination with the other component of Paxlovid, nirmatrelvir, as first treatment against MERS-CoV infection.
The research, carried out in Bristol’s School of Cellular and Molecular Medicine, used the instrument and platform, ImageXpress Pico Imaging System, purchased with support from the University’s Alumni and Friends to carry out the work.
Paper
‘Broad-spectrum antiviral activity of two structurally analogous CYP3A inhibitors against pathogenic human coronaviruses in vitro’ by Lara Gallucci, James Bazire, Andrew D Davidson, Iart Luca Shytaj in Antiviral Research [open access]
Further information
About coronavirus (SARS-CoV-2)
The surface of the coronavirus particle has proteins sticking out of it known as Spike proteins which are embedded in a membrane. They have the appearance of tiny little crowns, giving the virus its name (corona). Inside the membrane is the viral genome wrapped up in other proteins. The genome contains all the genetic instruction to mass produce the virus. Once the virus attaches to the outside of a human cell, its membrane fuses with the human cell membrane and its genetic information into the human cell. Next, the virus instructs the cell to start replicating its genome and produce its proteins. These are then assembled into many new copies of the virus which, upon release, can infect many more cells. The viral proteins play diverse further roles in coronavirus pathology.
Bristol UNCOVER Group
In response to the COVID-19 crisis, researchers at the University of Bristol formed the Bristol COVID Emergency Research Group (UNCOVER) to pool resources, capacities and research efforts to combat this infection.
Bristol UNCOVER includes clinicians, immunologists, virologists, synthetic biologists, aerosol scientists, epidemiologists and mathematical modellers and has links to behavioural and social scientists, ethicists and lawyers.
For more information about the University of Bristol’s to the coronavirus pandemic visit: www.bristol.ac.uk/research/impact/coronavirus/
Contact:
Joanne Fryer
Media & PR Manager - Research (Faculties of Health and Life Sciences)
Media Team
Communications Division
University of Bristol
Joanne.Fryer@bristol.ac.uk
Caroline Clancy (My pronouns are she/her)
PR & Media Manager (Research for Faculties of Health and Life Sciences)
Media Team
Communications Division
University of Bristol
31 Great George Street
Bristol
BS1 5QD
Tel: 07776 170238 (mobile)
Email: caroline.clancy@bristol.ac.uk
Source: https://www.bristol.ac.uk/news/2023/december/hiv-drug-coronaviruses.html
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