The lightbulb moment behind a potential antiviral advance

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An unexpected observation by a University of Queensland researcher could lead to a new treatment for deadly infectious diseases including COVID‑19, pneumonia in infants and children, or viral infections caused by Ebola and hantavirus. UQ neuroscientist and biochemist Dr Merja Joensuu, said the idea came while working on unrelated research.

News release

From: The University of Queensland

An unexpected observation by a University of Queensland researcher could lead to a new treatment for deadly infectious diseases including COVID‑19, pneumonia in infants and children, or viral infections caused by Ebola and hantavirus.

UQ neuroscientist and biochemist Dr Merja Joensuu, said the idea came while working on unrelated research.

“We were studying how certain processes work inside the human brain when I noticed a disruption in a pathway that numerous human viruses rely on to spread from one cell to the next,” Dr Joensuu, from UQ’s Australian Institute for Bioengineering and Nanotechnology said.

“That was the lightbulb moment.

“We realised that if we interfere with that pathway, we might be able to stop viruses from forming properly.”

With her collaborator Professor Giuseppe Balistreri from the University of Helsinki, the research team searched for a compound that could inhibit this pathway and found one currently being trialled as a cancer treatment.

Human enzyme N‑myristoyltransferase 1 (NMT1), which helps direct where proteins are located and how they function within human cells, was the compound’s target.

“Viruses can’t reproduce on their own, so they hijack human cells to make new copies,” Professor Balistreri said.

“This drug disrupts how the cell functions, causing new viruses to be assembled incorrectly.

“The virus doesn’t know this and keeps making and releasing less-effective versions of itself, which would give the immune system time to clean up the infection,” he said.

In laboratory studies, the researchers tested the drug against a range of viruses in cell cultures including SARS‑CoV‑2 (which causes COVID‑19), respiratory syncytial virus, a major cause of pneumonia in infants, and vesicular stomatitis virus, which causes disease in cattle, horses and occasionally humans.

They found infection levels dropped by about half after 1 day, and by up to 90 per cent after 2 days.

“The reduction is quite striking,” Dr Joensuu said.

“The study also suggests this strategy could potentially work on viruses with high mortality rates and long incubation time like Ebola and hantavirus.

“All viruses rely on exploiting host cell processes to replicate and spread.

“Because we are interfering with the host cell instead of directly targeting the virus, there is less chance of it mutating and building resistance to the drug.”

Researchers emphasised the drug is not yet approved for this use, with further studies needed to confirm safety and effectiveness, but Dr Joensuu said it showed a lot of promise.

“You can imagine that this could be a very effective antiviral, for example with treating respiratory conditions, used in the form of a nasal spray or an inhaler,” she said.

Read the research is published in Nature Communications.

Collaboration and acknowledgements

This research was supported by the facilities and staff at the Centre for Microscopy and Microanalysis and the Queensland Node of Metabolomics and Proteomics Australia, both of which are housed at the AIBN and funded the Australian Government’s National Collaborative Research Infrastructure Strategy (NCRIS).

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Media Release The University of Queensland, Web page
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Nature Communications
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Organisation/s: The University of Queensland, Assiut University, University of Helsinki, Medical University of Gdansk, Finnish Food Authority. The Francis Crick Institute, Imperial College London, Myricx Bio, i-Synapse
Funder: This work is supported by The UQ’s Amplify Fellowship (M.J.), The Research Council of Finland (335527), the European Union’s Horizon Europe Research and Innovation Program (101057553), the Helsinki Institute for Life Sciences (HiLIFE) Grants, and the Sigrid Juselius Foundation Senior Investigator Award (G.B.), WestPac Future Leaders Scholarship and The Australian Government Research Training Program (RTP) Scholarship (N.Y.), RTP (S.H.S), Instrumentarium Science Foundation Grant (240024) (R.O.), PREPARE-TID and VEO (European Union’s Horizon 2020; grant number 101137132, 874735) (T.S. and R.K.) and Sigrid Juselius Foundation 2022-2025 (T.S.), as well as Research Council of Finland (351010) and Jane and Aatos Erkko foundation and Helsinki University Hospital funds (O.V.). Q-MAP is supported by Bioplatforms Australia, an NCRIS-funded initiative. This work was also supported by an ARC Linkage Infrastructure, Equipment, and Facilities grant (LE130100078 and LE230100048). W.W.K. and E.W.T. acknowledge support from Myricx Pharma Ltd and Cancer Research UK, with support from the Engineering & Physical Sciences Research Council (C29637/A21451, C29637/A20183 and DRCNPG-Nov21\100001 to E.W.T.). Work in E.W.T.’s laboratories are supported by the Francis Crick Institute, which receives its core funding from Cancer Research UK, the UK Medical Research Council and the Wellcome Trust (FC001057 and FC001097).
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