Aug. 21 : Scientists at St. Jude Children’s Research Hospital have uncovered key differences between bird flu and human flu viruses.

The researchers used a mathematical technique, and identified specific amino acid building blocks that were statistically more likely to appear in avian influenza and human influenza virus proteins respectively.

According to them, the differences in these amino acids may be used as markers to track changes in H5N1 avian influenza strains that threaten humans.

“Influenza mutates rapidly, so that any marker that is not the same in bird flu but remains stable in human flu is likely to be important,” said Dr. David Finkelstein, Research Rssociate, the St. Jude Hartwell Center for Bioinformatics and Biotechnology.

“If human specific markers start accumulating in bird flu viruses that infect humans, that suggests that the bird flu may be adapting to humans and could spread,” he added.

It was also found that various strains of the H5N1 that had infected humans were more likely to contain human markers, as compared to those strains of the virus that had not infected humans.

The researchers, however, admitted to not having any evidence that the human markers in H5N1 and other avian influenza viruses directly contributed to the ability of these viruses to cause pandemics among humans, or that H5N1 was not any more adapted to humans.

During the study, the research team identified 32 specific locations in proteins where a gene mutation caused the existing amino acid to be substituted with a different amino acid. What made these 32 changes special was that influenza from birds differed from the influenza that was in humans.

When the avian influenza infected humans the amino acid changes were stable in the proteins and remained stable over time, an observation which prompted the researchers to think that those markers could be used to distinguish influenza viruses that infect birds from those that infect humans.

The researchers discovered these markers by computationally surveying the sequence of amino acids in 10,671 proteins from avian influenza viruses, and 13,757 proteins from human influenza viruses. The survey identified 32 persistent markers that exist in five bird and human virus proteins: PA, NP, M1, NS1 and PB2.

The markers identified stand out as obvious differences between bird and human viruses, and many appear in regions where host protein and viral replication occur. The researchers did not determine what functional role the markers play in the life of the viruses.

When the researchers studied markers in influenza viruses that caused pandemics in 1918, 1957 and 1968, they found that 13 of the 32 markers identified had remained stable in those viruses, and, just like the other viruses, those markers were distributed among PB2, PA, NP and M1—the proteins linked to virus replication.

“This suggests that these 13 sites are required for pandemic influenza to fully function,” Finkelstein said.

The study also highlighted that the H1N1 virus that caused the 1918 pandemic, the most deadly pandemic known, already contained 13 of the 32 markers early in the outbreak, and acquired the other 19 markers within 10 to 20 years, acquiring the preferred human influenza amino acids in stages. Eventually, descendents of the pandemic virus became the seasonal flu outbreaks rather than deadly pandemics.

“While we can’t directly estimate how long it would take an avian virus such as H5N1 to acquire these traits, we can use these markers to roughly measure the distance between an avian influenza and a pandemic,” said Dr. Clayton Naeve, St. Jude Hartwell Center director and senior author of the paper published in the online edition of the Journal of Virology. (ANI)

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