Tamiflu-resistant swine flu is turning up in about 2 percent of cases globally, researchers in Australia found, raising the risk that Roche Holding AG’s pill may become ineffective in fighting the pandemic H1N1 virus.
Drug resistance in the flu strain that sparked the 2009 influenza pandemic is being detected in virus samples collected from patients who haven’t been treated with Tamiflu, suggesting the mutant germs have spread, said Aeron Hurt, head of antiviral susceptibility research at the World Health Organization’s Collaborating Centre for Reference and Research on Influenza in Melbourne.
A Tamiflu-resistant clone of an older, seasonal flu strain took a year to become the dominant H1N1 virus globally. Swine flu may follow the same path, leaving doctors without their preferred treatment for influenza.
“That appears to be a larger risk now than it did at the start of the pandemic,” Hurt said in a telephone interview.’’
Hurt is presenting the research today at the Annual Scientific Meeting of the Australasian Society for Infectious Diseases in Canberra.
GlaxoSmithKline Plc’s inhaled Relenza drug is effective against the mutant strain, which causes the same symptoms as drug-sensitive flu.
Tamiflu, also known by its chemical name oseltamivir, and Relenza, an inhaled powder, reduce the severity and the duration of flu symptoms by 24 to 30 hours if treatment is started within the first two days of illness, according to the companies. Both drugs work by blocking a protein on the surface of influenza particles called neuraminidase, which allows the virus to spread from infected cells to other cells.
“Rates of Tamiflu resistance remain low globally although Roche takes the issue of resistance very seriously and collaborates with international organizations and authorities to monitor the situation,” said Daniel Grotzky, a spokesman for the drugmaker.
Tokyo-based Daiichi Sankyo Co. and BioCryst Pharmaceuticals Inc., based in Durham, North Carolina, have developed or are developing alternative neuraminidase inhibitors.
Mutant H1N1 viruses evade Tamiflu through a single genetic change known as the H275Y mutation which prevents the medicine from clinging to neuraminidase. In the past, the mutation has compromised the virus’s fitness, making it less likely to spread.
Hurt, who was among a group of scientists that reported a cluster of Tamiflu-resistant cases in eastern Australia in 2011, found other genetic changes have simultaneously occurred in the virus to enable the drug-repelling germ to retain its fitness.
Studies have shown that Tamiflu-resistant bugs develop sporadically in 0.4 percent to 4 percent of adults and children treated for seasonal influenza, according to Basel, Switzerland-based Roche.