# 4137
A fascinating report today (of course, press releases are designed to be fascinating . . . ) that outlines research at the University of California – Berkeley that shows that the genetic makeup of the H1N1 virus’s polymerase is different from any human-adapted influenza viruses studied to date.
The polymerase is an important segment in the influenza virus responsible for the virus's replication.
Previously known human-adapted influenza viruses all made a specific mutation in their polymerase to enable them to replicate efficiently in a human host.
The novel H1N1 virus didn’t. It retains an avian-adapted polymerase.
Instead it made a completely different mutation that allows the avian polymerase to replicate in a mammalian host.
As these researchers remind us, the H1N1 virus may not be through mutating and adapting to humans.
I’ve only reproduced part of this press release. Follow the link to read it in its entirety. Warning: Some of it is for hardcore science geeks.
H1N1 influenza adopted novel strategy to move from birds to humans
Bird influenza viruses have a variety of strategies to cross the species barrier and spread
The 2009 H1N1 influenza virus used a new strategy to cross from birds into humans, a warning that it has more than one trick up its sleeve to jump the species barrier and become virulent.
In a report in this week's early online edition of the journal Proceedings of the National Academy of Sciences, University of California, Berkeley, researchers show that the H1N1, or swine flu, virus adopted a new mutation in one of its genes distinct from the mutations found in previous flu viruses, including those responsible for the Spanish influenza pandemic of 1918, the "Asian" flu pandemic in 1957 and the "Hong Kong" pandemic of 1968.
Previous influenza strains that crossed from birds into people had a specific point mutation in the bird virus's polymerase gene that allowed the protein to operate efficiently inside humans as well. The polymerase transcribes the virus's RNA, allowing the host to express viral genes, and also copies the viral genome, needed to make new viruses.
The 2009 H1N1 virus retains the bird version of the polymerase, but has a second mutation that seems to suppress the ability of human cells to prevent the bird polymerase from working.
"We were quite shocked when we looked at the swine flu virus, which was clearly replicating in people and other mammalian systems, yet had a polymerase that looked like it was derived from a bird virus, which should not function too well in a human cell type," said UC Berkeley post-doctoral fellow Andrew Mehle of the Department of Molecular and Cell Biology. "The other mutation within the polymerase seems to compensate and allow the enzyme to function."
The researchers also discovered another strategy – one not yet adopted by any known flu virus – by which influenza virus can increase its virulence even more. When a particular human subunit is substituted for one of the three protein subunits that make up the bird polymerase, the new combination makes the polymerase more efficient in human cells.
"This is an extremely rare mutation and a rare combination, which suggests that there may be other ways that haven't emerged yet that these viruses are going to continue to evolve," said Jennifer Doudna, UC Berkeley professor of molecular and cell biology and an investigator in the Howard Hughes Medical Institute.
