Like all organisms, flu viruses must constantly adapt in order to survive in new surroundings. While well adapted to avian hosts, bird flu viruses (like H7N9, H5N1, H5N6) can occasionally jump to humans (and other mammals), whose physiology can present barriers to its spread and survival.
But flu viruses have a secret weapon.As they replicate in a host, they generate millions of copies in a few short hours. Since flu viruses are notoriously sloppy replicators, they make numerous mistakes. Most of these faulty copies are evolutionary failures and fall by the wayside, but occasionally a new mutation will appear that is better suited to the new host.
Host adapted viruses are more likely to replicate and survive, and over time, can become dominant and even `fixed' in the virus.As long as humans remain a dead end host (i.e. they don't transmit efficiently to other humans) for avian flu, the biggest danger is to the health of the infected individual. But should these viruses gain the ability to transmit efficiently, then the real problems begin.
While we often see reports of `mammalian adaptations' in H7N9, or mutations that favor anti-viral resistance, our understanding of exactly when (and where) these mutations are spawned is still lacking.Adding to our knowledge today, we've a new, open access study, published in the Journal of Infectious Diseases, which looks at the evolution of H7N9 in 11 subjects during the course of their infection.
Today's report focuses on 3 mutations we've seen often in the past;
- NA R292K which can provide resistance not only to oseltamivir, but to zanamivir and peramivir as well (see EID Journal: R292K Substitution & Antiviral Resistance)
- PB2 E627K which enables an influenza virus to replicate at the lower temperatures (roughly 33C) normally found in the upper human respiratory tract (see Eurosurveillance: Genetic Analysis Of Novel H7N9 Virus)
- and PB2 D701N (see Dual E627K and D701N mutations in the PB2 protein of A(H7N9) influenza virus increased its virulence in mammalian models)