Institute of Laboratory Animal Sciences, Chinese Academy of Medical Sciences (CAMS) & Comparative Medicine Center, Peking Union Medical Collage (PUMC), Key Laboratory of Human Disease Comparative Medicine, Ministry of Health, Pan Jia Yuan Nan Li No. 5, Chao Yang District, Beijing, China.
State Key Laboratory for Emerging Infectious Diseases, Department of Microbiology and the Research Centre of Infection and Immunology, The University of Hong Kong, Hong Kong SAR, China.
Institute of Laboratory Animal Sciences, Chinese Academy of Medical Sciences (CAMS) & Comparative Medicine Center, Peking Union Medical Collage (PUMC), Key Laboratory of Human Disease Comparative Medicine, Ministry of Health, Pan Jia Yuan Nan Li No. 5, Chao Yang District, Beijing, China. Electronic address: [email protected].
How the H7N9 avian influenza virus gained the distinct ability to infect humans is unclear. Pigs are an important host in influenza virus ecology because they are susceptible to infection with both avian and human influenza viruses and are often involved in interspecies transmission. Here, we passaged one avian isolate and one human isolate in pigs to examine the mammalian host adaptation of the H7N9 virus. The avian virus replicated to a high titer after one passage, whereas the human isolate replicated poorly after three passages in pig lungs. Sequence analysis found nine substitutions in the HA, NA, M and NS segments of the avian isolate, which enhanced the binding affinity for human-type receptors. These results indicate that avian H7N9 influenza viruses can be easily adapted to pigs and that pigs may act as an important intermediate host for the reassortment and transmission of such novel viruses.
AdaptationH7N9 influenza virusMutationPigReceptor bindingAdaptation, PhysiologicalAnimalsBirdsHumansInfluenza A Virus, H7N9 SubtypeInfluenza in BirdsInfluenza, HumanOrthomyxoviridae InfectionsSus scrofaSwineSwine Diseases
Structured evidence records
Evidence records
5 total
Host Range Experiment2 records
Host Range ExperimentExtraction confidence 0.90
Key finding
An avian isolate of H7N9 influenza virus replicated to high titer after one passage in pigs, demonstrating effective adaptation to the pig host.
Here, we passaged one avian isolate and one human isolate in pigs to examine the mammalian host adaptation of the H7N9 virus. The avian virus replicated to a high titer after one passage, whereas the human isolate replicated poorly after three passages in pig lungs.
Method
passage experiment; replication assay
Sample type
lungs
Experimental system
in vivo animal experiment
Host Range ExperimentExtraction confidence 0.90
Key finding
A human isolate of H7N9 influenza virus replicated poorly after three passages in pigs, indicating limited adaptation to the pig host.
Here, we passaged one avian isolate and one human isolate in pigs to examine the mammalian host adaptation of the H7N9 virus. The avian virus replicated to a high titer after one passage, whereas the human isolate replicated poorly after three passages in pig lungs.
Method
passage experiment; replication assay
Sample type
lungs
Experimental system
in vivo animal experiment
Cross Species Transmission1 records
Cross Species TransmissionExtraction confidence 0.80
Key finding
An avian H7N9 influenza virus replicated efficiently in pigs after a single passage, demonstrating bird-to-pig cross-species transmission and adaptation.
Here, we passaged one avian isolate and one human isolate in pigs to examine the mammalian host adaptation of the H7N9 virus. The avian virus replicated to a high titer after one passage, whereas the human isolate replicated poorly after three passages in pig lungs.
Sequence analysis found nine substitutions in the HA, NA, M and NS segments of the avian isolate, which enhanced the binding affinity for human-type receptors.
Genes or proteins
HA; NA; M; NS
Receptors
human-type receptors
Mechanism types
receptor_binding; host_adaptation
Receptor Usage1 records
Receptor UsageExtraction confidence 0.85
Key finding
Passaging of an avian H7N9 influenza isolate in pigs resulted in mutations that increased its binding affinity for human-type receptors.
Sequence analysis found nine substitutions in the HA, NA, M and NS segments of the avian isolate, which enhanced the binding affinity for human-type receptors.