Biochemists in the United States believe they may have found the Achilles heel of the H5N1 virus – and not just of the bird flu pathogen but of a wide range of other influenza strains.
The potential target is a long, flexible protein tail that is essential for virus replication, they reported on Thursday in Nature, the weekly British science journal.
The so-called nucleoprotein (NP) plays its role after a virus has hijacked a host cell and subverted it into a virus-making factory.
The NPs come together in small rings, stacking up one atop the other to form a column. The virus’ RNA genome twists around this column before being shipped out of the cell in copies that go on to infect other cells.
The team, led by Yizhi Jane Tao of Rice University in Houston, Texas, believe the weak point is the tail’s loop.
Just a single mutation in the amino acids comprising the loop is enough to prevent the NPs from forming the building blocks.
“We know from previous genetic studies that this tail loop is almost identifiable across strains of influenza A, so drugs that target the tail have a high potential of being effective across multiple strains, including the H5N1 strains,” a Rice University press release quoted Tao as saying.
“Such new antivirals are especially needed at the moment as some H5N1 viruses are resistant to the flu drug Tamiflu.”
Tamiflu is being stockpiled around the world as part of measures aimed at combating any pandemic flu virus that emerges from H5N1, which at present only uses birds as a host.
Influenza A is a group of flu viruses that include H5N1, seasonal flu as well as Hong Kong flu and Spanish flu, which caused two deadly pandemics last century.