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Research Article
Homologous recombination as an evolutionary force in the avian influenza A virus
Cheng-Qiang He1,*, Zhi-Xun Xie2,*, Guan-Zhu Han1, Jian-Bao Dong2, Dong Wang1, Jia-Bo Liu2, Le-Yuan Ma1, Xiao-Fei Tang2, Xi-Ping Liu1, Yao-Shan Pang2 and Guo-Rong Li1
1 College of Life Science, Shandong Normal University, Jinan, China 250014
2 Guangxi Veterinary Research Institute, Nanning, China 530001
* Corresponding authors: Cheng-Qiang He, College of Life Science, Shandong Normal University, Shandong Province, China 250014, Tel.: 86-531-8618-0745, E-mail: hchqiang@yahoo.com.cn ; Zhi-Xun Xie, Guangxi Veterinary Research Institute, Nanning, China 530001, Tel.: 86-771-3105702, Email: xiezhixun@126.com.
Received for publication August 7, 2008. Revision received September 27, 2008. Revision received October 8, 2008. Accepted for publication October 12, 2008.
Avian influenza A viruses (AIVs), including the H5N1, H9N2 and H7N7 subtypes, have been directly transmitted to humans, raising concerns over the possibility of a new influenza pandemic. To prevent a future avian influenza pandemic, it is very important to fully understand the molecular basis driving the change in AIV virulence and host tropism. Although virulent variants of other viruses have been generated by homologous recombination, the occurrence of homologous recombination within AIV segments is controversial and far from proven. This study reports three circulating H9N2 AIVs with similar mosaic PA genes descended from H9N2 and H5N1. Additionally, many homologous recombinants are also found deposited in GenBank. Recombination events can occur in PB2, PB1, PA, HA and NP segments and between lineages of the same/different serotype. These results collectively demonstrate that intragenic recombination plays a role in driving the evolution of AIVs, potentially resulting in effects on AIV virulence and host tropism changes.
MBE Advance Access published on October 17, 2008.
doi:10.1093/molbev/msn238
Homologous recombination as an evolutionary force in the avian influenza A virus
Cheng-Qiang He1,*, Zhi-Xun Xie2,*, Guan-Zhu Han1, Jian-Bao Dong2, Dong Wang1, Jia-Bo Liu2, Le-Yuan Ma1, Xiao-Fei Tang2, Xi-Ping Liu1, Yao-Shan Pang2 and Guo-Rong Li1
1 College of Life Science, Shandong Normal University, Jinan, China 250014
2 Guangxi Veterinary Research Institute, Nanning, China 530001
* Corresponding authors: Cheng-Qiang He, College of Life Science, Shandong Normal University, Shandong Province, China 250014, Tel.: 86-531-8618-0745, E-mail: hchqiang@yahoo.com.cn ; Zhi-Xun Xie, Guangxi Veterinary Research Institute, Nanning, China 530001, Tel.: 86-771-3105702, Email: xiezhixun@126.com.
Received for publication August 7, 2008. Revision received September 27, 2008. Revision received October 8, 2008. Accepted for publication October 12, 2008.
Avian influenza A viruses (AIVs), including the H5N1, H9N2 and H7N7 subtypes, have been directly transmitted to humans, raising concerns over the possibility of a new influenza pandemic. To prevent a future avian influenza pandemic, it is very important to fully understand the molecular basis driving the change in AIV virulence and host tropism. Although virulent variants of other viruses have been generated by homologous recombination, the occurrence of homologous recombination within AIV segments is controversial and far from proven. This study reports three circulating H9N2 AIVs with similar mosaic PA genes descended from H9N2 and H5N1. Additionally, many homologous recombinants are also found deposited in GenBank. Recombination events can occur in PB2, PB1, PA, HA and NP segments and between lineages of the same/different serotype. These results collectively demonstrate that intragenic recombination plays a role in driving the evolution of AIVs, potentially resulting in effects on AIV virulence and host tropism changes.
MBE Advance Access published on October 17, 2008.
doi:10.1093/molbev/msn238
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