Pandemic Seasonal H1N1 Reassortants Recovered from Patient Material Display a Phenotype Similar to That of the Seasonal Parent.
We have previously shown that 11 patients became naturally coinfected with seasonal H1N1 (A/H1N1) and pandemic H1N1 (pdm/H1N1) during the Southern hemisphere winter of 2009 in New Zealand. Reassortment of influenza A viruses is readily observed during coinfection of host animals and in vitro; however, reports of reassortment occurring naturally in humans are rare. Using clinical specimen material, we show reassortment between the two coinfecting viruses occurred with high likelihood directly in one of the previously identified patients. Despite the lack of spread of these reassortants in the community, we did not find them to be attenuated in several model systems for viral replication and virus transmission: multistep growth curves in differentiated human bronchial epithelial cells revealed no growth deficiency in six recovered reassortants compared to A/H1N1 and pdm/H1N1 isolates. Two reassortant viruses were assessed in ferrets and showed transmission to aerosol contacts. This study demonstrates that influenza virus reassortants can arise in naturally coinfected patients.



Reassortment of influenza A viruses is an important driver of virus evolution, but little has been done to address humans as hosts for the generation of novel influenza viruses. We show here that multiple reassortant viruses were generated during natural coinfection of a patient with pandemic H1N1 (2009) and seasonal H1N1 influenza A viruses. Though apparently fit in model systems, these reassortants did not become established in the wider population, presumably due to herd immunity against their seasonal H1 antigen.
St. Jude Children's Research Hospital, Memphis, Tennessee, USA steph.sonnberg@takeda.com.
Stephanie
S
Sonnberg
St. Jude Children's Research Hospital, Memphis, Tennessee, USA.
Mariette F
MF
Ducatez
St. Jude Children's Research Hospital, Memphis, Tennessee, USA.
Jennifer
J
DeBeauchamp
St. Jude Children's Research Hospital, Memphis, Tennessee, USA.
Jeri-Carol
JC
Crumpton
St. Jude Children's Research Hospital, Memphis, Tennessee, USA.
Adam
A
Rubrum
St. Jude Children's Research Hospital, Memphis, Tennessee, USA.
Bridgett
B
Sharp
Institute of Environmental Science and Research, Upper Hutt, New Zealand.
Richard J
RJ
Hall
Institute of Environmental Science and Research, Upper Hutt, New Zealand.
Matthew
M
Peacey
Institute of Environmental Science and Research, Upper Hutt, New Zealand.
Sue
S
Huang
St. Jude Children's Research Hospital, Memphis, Tennessee, USA.
Richard J
RJ
Webby
D000818:Animals; D060085:Coinfection / Q000821:virology*; D004195:Disease Models, Animal; D004847:Epithelial Cells / Q000821:virology; D005289:Ferrets; D006801:Humans; D053118:Influenza A Virus, H1N1 Subtype / Q000235:genetics* / Q000254:growth & development* / Q000302:isolation & purification; D007251:Influenza, Human / Q000821:virology*; D009520:New Zealand; D009976:Orthomyxoviridae Infections / Q000635:transmission / Q000821:virology; D010641:Phenotype; D016865:Reassortant Viruses / Q000235:genetics* / Q000254:growth & development* / Q000302:isolation & purification; D014774:Virulence; D014779:Virus Replication