Bloomberg News

Tamiflu-Resistance Gene in H7N9 Bird Flu Spurs Drug Tests

April 11, 2013

Tamiflu-Resistance Gene in H7N9 Spurs Drug-Sensitivity Inquiry

An undated handout photograph shows GlaxoSmithKline Plc's Relenza, provided to the media on Dec. 10, 2008. Source: GlaxoSmithKline Plc via Bloomberg

A gene mutation known to help influenza resist Tamiflu was found in the first of three H7N9 bird-flu patient specimens in China, sequence data show.

The flu virus from the patient in Shanghai has a mutation known as R292K that causes high-level resistance to the Roche Holding AG (ROG) pill and reduced sensitivity to a related drug from GlaxoSmithKline Plc (GSK) called Relenza, genetic sequence information posted on the website of the Global Initiative on Sharing Avian Influenza Data show. Subsequent H7N9 specimens from a patient in Shanghai and one in Anhui province don’t show the mutation.

The finding of the mutation warrants further analysis, said Masato Tashiro, a director at Japan’s National Institute of Infectious Diseases in Tokyo. Preliminary tests so far show no evidence that the new flu strain, which has sickened at least 33 people, killing nine, in eastern China, has developed resistance to the neuraminidase inhibitor drugs Tamiflu and Relenza, the World Health Organization said in a statement yesterday.

“When you look at the raw data and compare the three strains of the virus, there’s a signal from one strain that it’s less sensitive to both of the neuraminidase inhibitors,” Tashiro said in a telephone interview. “It’s not a strong signal, but there’s a possibility” of resistance, he said.

The Chinese Center for Disease Control and Prevention in Beijing has studied H7N9 specimens and confirmed that the virus is sensitive to neuraminidase inhibitors, Tashiro said.

“At this point, we should accept what the Chinese CDC says,” he said.

More experiments are needed to understand the biological significance of gene sequence data, said Gavin Smith, an associate professor in the emerging infectious diseases program at Singapore’s Duke-NUS medical school.

Absence of the R292K mutations “would be of less concern than having them there, but it still needs to be tested,” said Smith. “They provide an indication of the type of things we should be looking at.”

To contact the reporters on this story: Kanoko Matsuyama in Tokyo at kmatsuyama2@bloomberg.net; Jason Gale in Melbourne at j.gale@bloomberg.net

To contact the editor responsible for this story: Jason Gale at j.gale@bloomberg.net


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