In my last blog, I discussed a laboratory reassortment between H5N1 and H3N2 that resulted in deadly hybrids. In case anyone was wondering if this was a fluke, it wasn’t.
Another group of scientists performed a ressortment experiment between a H5N1 strain (A/Goose/Guandong/1/96) and another avian flu virus, H7N1 (A/FPV/Rostok/34). To the experimenters’ surprise, a hybrid strain with the NS genomic segment from H5N1 and the other 7 genomic segments from H7N1, was able to immediately replicate in human cells, without any adaptation. Further, the NS exchange transformed a normally benign H7N1 virus into a lethal strain.
From the study:
The AIV A/FPV/Rostok/34 (H7N1) is known to be apathogenic for mice. We therefore investigated whether the reassortment FPV NS GD differs in this respect. In the first set of experiments, 8-week-old female C57BL/6 mice were intranasally infected with either virus at various doses in a range 10(2) to 10(6) PFU. As expected, none of the animals infected with rFPV developed influenza-specific disease symptoms (e.g., weight loss or apathetic behavior). In contrast, mice infected with FPV NS GD at concentrations of 10(4), 10(5), or 10(6) PFU developed disease, and 10 to 30% of the mice died…
…the reassortant FPV NS GD, which differs from the rFPV only by the NS segment, replicated to high titers in embryonated chicken eggs, and it seemed to be more pathogenic. Interestingly, it was able to replicate more efficiently in human cell lines, in primary mouse AESs, and in mice without previous adaptation.
The NS genomic segment is suspected to be involved in the virulence of some flu strains from other experiments. What is noteworthy from this study is that a simple exchange of this one genomic segment from one flu virus to another immediately leads to greater virulence, without any further adaptation.
A new, more deadly flu virus could arise at any time, with no warning.
And it could happen in more than one way.
Ma et al. (2010) The NS segment of an H5N1 highly pathogenic avian influenza virus (HPAIV) is sufficient to alter replication efficiency, cell tropism, and host range of an H7N1 HPAIV. J. Virol.