Thursday, July 10, 2014

J. Virol: Continued Reassortment Of Swine Flu Viruses With Genes From pH1N1 In China



# 8820


Big changes in influenza viruses – the kind that can create a novel, and potentially pandemic producing strain – come about through antigenic shift, also known as reassortment.  For shift to occur, two different flu strains must infect the same host simultaneously, and swap one or more gene segments.


Most reassortant viruses are evolutionary failures, but every once in awhile a more `fit’ virus emerges.


While seemingly an unlikely confluence of events – for pigs - who number in the millions, live in close quarters, have frequent contact with other pigs, birds, and humans, and who are notoriously susceptible to flu – shift happens with surprising frequency.


Reassortant pig[6]

Since pigs can be infected by more than one flu virus at the same time, it is possible for two viruses to swap genetic material (reassort), resulting in a new hybrid strain.


Here in North America we’ve been watching the evolution of several swine variant viruses (H1N1v, H1N2v, H3N2v) over the past few years, all of which have reassorted with - and picked up the M gene segment from – the 2009 H1N1 virus (see Keeping Our Eyes On The Prize Pig).


Although reassortant flu viruses can emerge anywhere in the world (2009 H1N1 first emerged in North America), nowhere are pigs watched with more interest than in China, where huge populations of pigs are raised with frequent contact with other species, including humans.


Last year, in  EID Journal: Predicting Hotspots for Influenza Virus Reassortment, we saw China ranked as one of the globe’s top breeding grounds for new flu strains. 


Today we’ve a new paper, appearing in the Journal of Virology, that looks at the expanding diversity of reassorted swine flu viruses carrying genes from the 2009 H1N1 pandemic virus in Chinese pigs.  While the fully `humanized’ 2009 H1N1 virus doesn’t circulate in swine, researchers have isolated at least 17 reassortants  containing pH1N1-origin genes.


First the link and abstract, then I’ll have a bit more.



Expansion of genotypic diversity and establishment of 2009 H1N1 pandemic-origin internal genes in pigs in China

Huyi Lianga,b,c, Tommy Tsan-Yuk Lama,b,c, Xiaohui Fand, Xinchun Chena, Yu Zenga,c, Ji Zhoua,b,c, Lian Duana,b,c, Maying Tseb, Chung-Hei Chanb, Lifeng Lib,c, Tak-Ying Leungb, Chun-Hung Yipb, Chung-Lam Cheungb, Boping Zhoua, David K. Smithb,c, Leo Lit-Man Poona,b, Malik Peirisa,b, Yi Guana,b,c and Huachen Zhua,b,c


‘Two-way' transmission of influenza viruses between humans and swine has been frequently observed and the occurrence of the 2009 H1N1 pandemic influenza (pdm/09) demonstrated that swine-origin viruses could facilitate the genesis of a pandemic strain. Although multiple introductions to and reassortment in swine of the pdm/09 virus have been repeatedly reported in both Eurasia and the Americas, its long-term impact on the development of swine influenza viruses (SIVs) has not been systematically explored. Our comprehensive evolutionary studies on the complete genomes of 387 SIVs obtained from 2009 to 2012 in influenza surveillance in China revealed 17 reassortant genotypes with pdm/09-origin genes.

Even though the entire 2009 pandemic virus and its surface genes cannot persist, its internal genes have becoming established and are now the predominant lineages in pigs in the region. The main persistent pdm/09-origin reassortant forms had at least 5 pdm/09-origin internal genes and their surface genes primarily of European avian-like (EA) or human H3N2-like SIV origin. These findings represent a marked change to the evolutionary patterns and ecosystem of SIVs in China. It is possible that the pdm/09-origin internal genes may be in the process of replacing EA- or triple reassortant-like internal genes. These alterations to the SIV gene pool need to be continually monitored to assess changes in the potential for SIVs to transmit to humans.



Remarkably, in less than five years, the swine influenza virus (SIV) gene pool in China has been dramatically re-invented with the internal genes derived from the pH1N1 virus now dominant, and continuing to expand. 


While their surface genes (HA & NA) remain more or less stable, the acquisition of as many as 5 internal genes from an already `humanized’  flu virus is of concern.


The authors write:


Over the survey period, these internal genes became predominant, potentially replacing those of the enzootic SIV lineages. The altered diversity of the SIV gene pool needs to be closely monitored for changes in the potential of SIVs to transmit to humans.


Although with the emergence of H7N9, H10N8, and H5N8 our attentions have been focused more on avian influenzas these past couple of years, in truth, a reassortant virus could emerge from practically any species susceptible to multiple flu strains (see Study: Dogs As Potential `Mixing Vessels’ For Influenza, mBio: A Mammalian Adapted H3N8 In Seals ).


Historically, avian and swine influenzas have a track record of producing pandemic strains, and so we tend to watch both arenas with particularly interest. 


For more on influenza reassortment, you may wish to revisit:


Viral Reassortants: Rocking The Cradle Of Influenza
Study: Novel & Variant Swine Influenzas In Korean Pigs
Seroprevalence Study: Avian Flu In Chinese Pigs

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