Friday, September 16, 2011

Study: Reassorted H1N1-H5N1 Produced Virulent Strain




# 5846



Less than 3 weeks ago, in Professor Peter Doherty On Bird Flu, we looked at his concerns over the possibility that the H5N1 virus might one day swap genes (reassort) with the H1N1 virus and produce an easily transmitted, highly virulent flu strain.


Reassorted viruses can result when two different flu strains inhabit the same host (human or otherwise) at the same time. Under the right conditions, they can swap one or more gene segments and produce a hybrid virus.





While a bird flu reassortment has long been a concern, many scientists have assumed that such a genetic merger - with an already human–adapted flu virus - would produce a less virulent flu strain.


Something more on par with the (still horrific) 1918 Pandemic virus which killed about 2.5% of those stricken in the United States.


Today we’ve research that appears in The Journal of Virology that calls that assumption into question.



Increased pathogenicity of a reassortant 2009 pandemic H1N1 influenza virus containing an H5N1 hemagglutinin

J. Virol. doi:10.1128/JVI.05582-11

Troy D. Cline1, Erik A. Karlsson1, Pamela Freiden1, Bradley J. Seufzer1, Jerold E. Rehg2, Richard J. Webby1, and Stacey Schultz-Cherry1,*

1 Departments of Infectious Diseases
2 Pathology, St. Jude Children's Research Hospital, Memphis, TN 38105



Using reverse genetics, researchers at St. Jude Children’s Research Hospital created several reassortant 2009 pH1N1 viruses with individual genes borrowed from a 1997 H5N1 virus, and then tested them for replication and virulence.


They found that one of these lab-created viruses, with the HA gene from the H5 virus, increased replication over the parental strain and produced virulence in mice comparable to the parent H5N1 strain.


They also report that serial passage through human lung epithelial cells "resulted in increased pathogenicity, suggesting that these viruses may easily adapt to humans and become more virulent."

Somewhat surprisingly, the opposite was found when the parent H5N1 strain was passed sequentially through human lung cells, as the virus grew weaker.


CIDRAP has a news brief on this study here, and you can read the abstract here.


Of course, just because it can be artificially created in the laboratory doesn’t guarantee that it will evolve on its own in the wild. 


It just means that it’s possible.


The less-than-comforting bottom line from the abstract:


Together, these data suggest that reassortment between co-circulating human pH1N1 and avian H5N1 influenza strains may result in a virus with the potential for increased pathogenicity in mammals.


For more on the reassortment and mutation potential of influenza viruses, you may wish to revisit some of these earlier blogs:


M Is For Mutation
Two Reassortment Studies To Ponder
Hong Kong: Influenza Surveillance In Pigs
EID Journal: Swine Flu Reassortants In Pigs
If You’ve Seen One Triple Reassortant Swine Flu Virus . . .