Flu Virus binding to Receptor Cells – Credit CDC
With all of the attention being given to the H7 and H5 avian flu strains this winter (see The Transmission Potential Of A(H7N9) In China & WHO: H5 Currently The Most Obvious Avian Flu Threat) it is easy to forget there are other avian subtypes on our radar as well.
We’ve seen a handful of scattered H9N2 infections over the years, and even a one-off H6N1 in Taiwan in 2013. There’s a reservoir of mixed-host (avian, swine, equine, canine, etc.) H1, H2 & H3 viruses worthy of our attentions, as well.
But bringing up the rear are the H10 avian viruses, which have made a splash in the past few years.
Last fall, in Avian H10N7 Linked To Dead European Seals, we looked at the die off of thousands of harbor seals due to a combination of avian H10N7 influenza, pneumonia, and bacterial infection. While known human infections with avian H10 viruses are limited, we’ve discussed them previously on several occasions.
- In 2004, the first known human infections were reported among two Egyptian toddlers, as described in the WHO/CDS/CSR/RMD report Avian Influenza Virus A (H10N7) Circulating among Humans in Egypt.
- And again, in 2012, in EID Journal: Human Infection With H10N7 Avian Influenza, we looked at a limited outbreak among workers with only mild symptoms at a chicken farm in Australia.
- And perhaps most concerning, we saw three severe infections with an H10N8 virus in China last winter.
A little over a month ago, in TSRI: H10N8 and H6N1 Bind Poorly To Human Receptor Cells, we saw an encouraging report suggesting that neither subtype was poised to pose a serious pandemic threat, although they warned that these viruses bind differently than other avian viruses we’ve seen, and that our understanding of how these viruses mutate isn’t complete enough to warrant complacency.
All of which serves a prelude to a new study, published on April 8th in the Journal of Virology, that examines the genetic diversity, and behavior, of eight H10N8 viruses collected between 2009 and 2013.
- The genetic diversity (5 genotypes) detected among ducks and chickens
- Seven of the eight viruses replicated well in the lungs of mice
- Differences in virulence (in mice) between duck and chicken genotypes
- Dual binding to both Human (a2,6) and avian (a2,3) receptor cells, albeit with marked preference for avian receptors.
- The role that H9N2 has played in its evolution
The entire study, including an array of graphs and charts, is available at:
Guohua Denga, Jianzhong Shia, Jing Wanga, Huihui Konga, Pengfei Cuia, Fang Zhanga, Dan Tana, Yasuo Suzukib, Liling Liua, Yongping Jianga, Yuntao Guana and Hualan Chena⇑
We analyzed eight H10N8 viruses isolated from ducks and chickens in live poultry markets from 2009 to 2013 in China. These viruses showed distinct genetic diversity and formed five genotypes: the four duck isolates formed four different genotypes, whereas the four chicken viruses belong to a single genotype. The viruses bound to both human- and avian-type receptors, and four of the viruses caused 12.7% – 22.5% body weight loss in mice.
In summary, our genetic studies indicate that the four duck viruses belong to four different genotypes, suggesting that they were introduced into ducks independently; the four chicken viruses belong to one genotype and appear to be hybrids of a duck virus and the local H9N2 viruses (Table 1).
The ability of H10N8 viruses to bind to human-type receptors facilitates their infection of humans, as occurred with the H7N9 viruses (28).
The more efficient replication in mice of the viruses isolated in Jiangxi province than the three duck viruses isolated in Hunan province suggests that the internal genes of the H9N2 viruses may have further increased the replicative ability and virulence of H10N8 viruses in mammals; of cause, the surface proteins may have also contributed to the difference of the virulence.
Although the viruses in our studies were all isolated from healthy birds, two H10 influenza viruses, A/turkey/England/384/79 and A/mandarin duck/Singapore/805/F-72/7/93, were reported to be highly pathogenic in chickens (3, 30). Therefore, it is important to continue monitoring the evolution of H10N8 influenza viruses and to evaluate their potential to cause disease in poultry and pandemics in humans.
As we’ve seen with the H5N1 and H7N9 viruses, H10N8 continues to evolve and the ubiquitous H9N2 virus appears to play a substantial role in its evolution. An LPAI virus in chickens, H10N8 (like H7N9) can spread stealthily between flocks without the typical warning signs that HPAI viruses provide, making it more difficult to detect and eradicate.
While the general consensus is that the H10 family of avian viruses aren’t `ready for primetime’, H10N8 has already shown the ability to produce serious (even fatal) illness in humans, which elevates its profile when compared to many other less virulence avian strains.
Add in its growing genetic diversity, and its ability to reassort with other avian flu viruses, and H10N8 deservedly holds a second tier position on our list of avian flu viruses to watch.