, Science and Technology. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Competing Interests: The authors have declared that no competing interests exist. E-mail: [email protected] Introduction The 2009 pandemic influenza A virus, a new strain of virus identified in Mexico in April 2009, spread quickly among humans worldwide to cause the first influenza pandemic disease of the 21st century. As of April 2010, this swineorigin influenza virus had led to outbreaks on both local and global scales with severe consequences for human health and the global economy, resulting in about 18,000 deaths around the world. On August 10, 2010, the WHO announced that the 2009 pdm A influenza had moved into the post-pandemic period. In spite of this, however, localized outbreaks of various magnitudes continued. In fact, transmission of the 2009 pdm A influenza virus remained intense in certain parts of India and in the temperate southern hemisphere, particularly New Zealand and Australia. There are concerns that this virus may mutate or reassort with other existing influenza viruses to give rise to more readily transmittable or more pathogenic viruses. The 2009 pdm influenza virus is a triple combination comprising gene segments from both North American and Eurasian swine influenza and from avian influenza viruses. Namely, the 2009 pdm influenza A virus possesses PB2 April 2011 | Volume 6 | Issue 4 | e18956 2009 Pandemic Influenza A Virus in Japan and PA genes of North American avian virus origin, a PB1 gene of human H3N2 virus origin, HA, NP, and NS genes of classical swine virus origin, and NA and M genes of Eurasian avianlike swine virus origin. In this regard, the 2009 pdm influenza A virus is unique. 1796596-46-7 Unusual for influenza, the 2009 pdm influenza preferentially affected young adults and children, whereas elderly people generally showed preexisting immunity. The influenza virus envelope protein HA is a principal surface antigen. A comparison of amino acid sequences between the 2009 pdm A and previous influenza viruses revealed that the 2009 pdm A virus and the 1918 Spanish influenza viruses share some common signatures. The 2D1 antibody from a survivor of the 1918 Spanish flu neutralized both 1918 and 2009 pdm H1N1 viruses, suggesting that the antibody’s epitope is conserved in both pandemic viruses. Since the outbreak of the 2009 pdm A influenza infection, a large-scale surveillance was carried out at the molecular level, and the evolutionary and spatial dynamics of the 2009 pdm A virus have been well characterized to date. The virus genome was found to have an extremely high evolutionary rate. Phylogenetic analyses have shown that viruses in four major clusters have disseminated globally and cocirculated over time and space since April 2009. In Japan, the first 2009 pdm A influenza case was reported on May 9, 2009, and that was followed by more than 200 reported cases in the Osaka and Kobe areas by May 21, 2009. Thereafter, the pandemic infection spread widely throughout Japan, where the numbers of influenza cases reported per sentinel provider peaked at 39.63 in November 2009, with over 200 fatal cases due to infection with the 2009 pdm influenza viruses. Shiino et al. analyzed the molecular evolution of the 2009 pdm A virus to find that a major part of the 75 strains isolated in Japan could be differentiated into 12 micro-clades. Their analysis, however, was performed, Science and Technology. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Competing Interests: The authors have declared that no competing interests exist. E-mail: [email protected] Introduction The 2009 pandemic influenza A virus, a new strain of virus identified in Mexico in April 2009, spread quickly among humans worldwide to cause the first influenza pandemic disease of the 21st century. As of April 2010, this swineorigin influenza virus had led to outbreaks on both local and global scales with severe consequences for human health and the global economy, resulting in about 18,000 deaths around the world. On August 10, 2010, the WHO announced that the 2009 pdm A influenza had moved into the post-pandemic period. In spite of this, however, localized outbreaks of various magnitudes continued. In fact, transmission of the 2009 pdm A influenza virus remained intense in certain parts of India and in the temperate southern hemisphere, particularly New Zealand and Australia. There are concerns that this virus may mutate or reassort with other existing influenza viruses to give rise to more readily transmittable or more pathogenic viruses. The 2009 pdm influenza virus is a triple combination comprising gene segments from both North American and Eurasian swine influenza and from avian influenza viruses. Namely, the 2009 pdm influenza A virus possesses PB2 April 2011 | Volume 6 | Issue 4 | e18956 2009 Pandemic Influenza A Virus in Japan and PA genes of North American avian virus origin, a PB1 gene of human H3N2 virus origin, HA, NP, and NS genes of classical swine virus origin, and NA and M genes of Eurasian avianlike swine virus origin. In this regard, the 2009 pdm influenza A virus is unique. Unusual for influenza, the 2009 pdm influenza preferentially affected young adults and children, whereas elderly people generally showed preexisting immunity. The influenza virus envelope protein HA is a principal surface antigen. A comparison of amino acid sequences between the 2009 pdm A and previous influenza viruses revealed that the 2009 pdm A virus and the 1918 Spanish influenza viruses share some common signatures. The 2D1 antibody from a survivor of the 1918 Spanish flu neutralized both 1918 and 2009 pdm H1N1 viruses, suggesting that the antibody’s epitope is conserved in both pandemic viruses. Since the outbreak of the 2009 pdm A influenza infection, a large-scale surveillance was carried out at the molecular level, and the evolutionary and spatial dynamics of the 2009 pdm A virus have been well characterized to date. The virus genome was found to have an extremely high evolutionary rate. Phylogenetic analyses have shown that viruses 19774075 in four major clusters have disseminated globally and cocirculated over time and 
space since April 2009. In Japan, the first 2009 pdm A influenza case was reported on May 9, 2009, and that was followed by more than 200 reported cases in the Osaka and Kobe areas by May 21, 2009. Thereafter, the pandemic infection spread widely throughout Japan, where the numbers of influenza cases reported per sentinel provider peaked at 39.63 in November 2009, with over 200 fatal cases due to infection with the 2009 pdm influenza viruses. Shiino et al. analyzed the molecular evolution of the 2009 pdm A virus to find that a major part of the 75 strains isolated in Japan could be differentiated into 12 micro-clades. Their analysis, however, was performed
