HONG KONG, July 10 (Reuters) - Scientists have identified around 100 genes that the H5N1 bird flu virus needs in a host in order to replicate, and this finding may help in the hunt for ways to block its proliferation.
"All viruses rely on host cell proteins and their associated mechanisms to complete the viral life cycle. Identifying the host molecules that participate in each step of virus replication could provide valuable new targets for antiviral therapy," they wrote in the latest edition of Nature magazine.
In their study, the experts from Japan, Indonesia and the United States infected fruit fly cells with genetically altered H5N1 virus.
The H5N1 virus needed slight modifications because fruit flies are normally not susceptible to influenza.
The experts also chose the fruit fly because it has a relatively small number of genes -- 14,000 -- making it easier for scientists to study.
"We found genes (proteins) that are important for influenza virus replication. We identified about 100 genes," said Yoshihiro Kawaoka, a leading virologist and bird flu expert at the University of Tokyo in Japan.
Of these, at least three existed in human cells.
"We took three and tested them and they were important for flu virus replication (in humans)," he told Reuters.
"I presume that many of the other genes we identified are also important for influenza virus replication in humans."
Next, the team wants to zero in on host proteins that the H5N1 needs to bind to in order to replicate.
"If you could inhibit (block) the interaction between those (host) proteins and influenza virus proteins, you can inhibit virus replication. This can be a target for development of new drugs," Kawaoka said.
Although the H5N1 remains mainly a disease among birds, it has killed 243 of the 385 people it has infected since 2003.
Experts have warned for years now that it can trigger a pandemic killing millions of people if it ever becomes easily transmitted among humans.
Worse, it has also shown signs of developing resistance to the few available treatments. (Reporting by Tan Ee Lyn; Editing by David Fox)