Media Release | Feb. 21, 2013

New flu drug stops virus in its tracks

A new class of influenza drug has been shown effective against drug-resistant strains of the flu virus, according to a study led by University of British Columbia researchers.Published online today in the journal Science Express, the study details the development of a new drug candidate that prevents the flu virus from spreading from one cell to the next. The drug is shown to successfully treat mice with lethal strains of the flu virus.

In order to spread in the body, the flu virus first uses a protein, called hemagglutinin, to bind to the healthy cell’s receptors. Once it has inserted its RNA and replicated, the virus uses an enzyme, called neuraminidase, to sever the connection and move on to the next healthy cell.

“Our drug agent uses the same approach as current flu treatments – by preventing neuraminidase from cutting its ties with the infected cell,” says UBC Chemistry Prof. Steve Withers, the study’s senior author. “But our agent latches onto this enzyme like a broken key, stuck in a lock, rendering it useless.”

Watch a video of the flu virus at work at http://youtu.be/kSLRmj0APZw. (credit: CSIRO/Magicpics. Download this video)

The World Health Organization estimates that influenza affects three to five million people globally each year, causing 250,000 to 500,000 deaths. In some pandemic years, the figure rose to millions.

“One of the major challenges of the current flu treatments is that new strains of the flu virus are becoming resistant, leaving us vulnerable to the next pandemic,” says Withers, whose team includes researchers from Canada, the UK, and Australia.

“By taking advantage of the virus’s own ‘molecular machinery’ to attach itself,” Withers adds. “The new drug could remain effective longer, since resistant virus strains cannot arise without destroying their own mechanism for infection.”

NB: An animation and step-by-step cartoon of the new drug’s mechanism are available at http://www.publicaffairs.ubc.ca/?p=81569

 

BACKGROUND | NEW FLU DRUG

Partners and funders

The research is funded by the Canadian Institutes of Health Research, the Canada Foundation for Innovation, the British Columbia Knowledge Development Fund.

The research team includes scientists from UBC, Simon Fraser University, and Centre for Disease Control in B.C., the University of Bath in the U.K. and CSIRO Materials Science and Engineering in Australia.

The new drug technology was developed in collaboration with The Centre for Drug Research and Development (CDRD) and has been advanced into CDRD Ventures’ Inc., CDRD’s commercialization vehicle, in order to secure private sector partners and investors to develop it through clinical trials.

CDRD is Canada’s national drug development and commercialization centre, which provides expertise and infrastructure to enable researchers from leading health research institutions to advance promising early-stage drug candidates. CDRD’s mandate is to de-risk discoveries stemming from publicly-funded health research and transform them into viable investment opportunities for the private sector — thus successfully bridging the commercialization gap between academia and industry, and translating research discoveries into new therapies for patients.

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Prof. Stephen Withers
UBC Dept. of Chemistry
Tel: 604.822.3402
E-mail: withers@chem.ubc.ca

Brian Lin
UBC Public Affairs
Tel: 604.822.2234
Cell: 604.818.5685
E-mail: brian.lin@ubc.ca

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UBC Chemistry Prof. Steve Withers (credit: UBC)

UBC Chemistry Prof. Steve Withers (credit: UBC)

In order to spread in the body, the flu virus (blue) first uses a protein, called hemagglutinin, to bind to the receptors (green) on a healthy cell (red).

In order to spread in the body, the flu virus (blue) first uses a protein, called hemagglutinin, to bind to the receptors (green) on a healthy cell (red).

Once the flu virus has inserted its DNA into the healthy cell and replicated, it would remain stuck to the cell via its hemagglutinin if it were not for the neuraminidase enzyme, which severs the connection to the infected cell’s receptors.

Once the flu virus has inserted its DNA into the healthy cell and replicated, it would remain stuck to the cell via its hemagglutinin if it were not for the neuraminidase enzyme, which severs the connection to the infected cell’s receptors.

Current flu treatments work to inhibit the neuraminidase so the flu virus cannot move on to the next healthy cell.

Current flu treatments work to inhibit the neuraminidase so the flu virus cannot move on to the next healthy cell.

This is done through binding drug molecules into the neuraminidase, like a key into a lock, blocking it from its normal role.

This is done through binding drug molecules into the neuraminidase, like a key into a lock, blocking it from its normal role.

The virus remains bound to the infected cell.

The virus remains bound to the infected cell.

The immune system clears away the trapped flu viruses. (Credit: CSIRO/Magipics)

The immune system clears away the trapped flu viruses. (Credit: CSIRO/Magipics)

Life Cycle: This figure shows the life cycle of the flu virus and how the new flu drug agent prevents the virus from spreading from cell to cell by irreversibly inhibiting the action of the neuraminidase like a broken key stuck in a lock. (Credit: Tom Wennekes, UBC)

Life Cycle: This figure shows the life cycle of the flu virus and how the new flu drug agent prevents the virus from spreading from cell to cell by irreversibly inhibiting the action of the neuraminidase like a broken key stuck in a lock. (Credit: Tom Wennekes, UBC)

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