Foot-and-mouth disease (FMD) is a highly contagious viral disease characterized by rapid onset and high morbidity in a wide range of susceptible host species within the members of the order Artiodactyla (for reviews see [1, 2]). The disease is endemic in the Middle East, Central and South Asia, Africa, and some countries in South America. FMD is notifiable to the World Organisation for Animal Health (OIE) and as a consequence FMD-affected countries have restricted trade in livestock and livestock products with FMD-free regions and countries. Therefore, an incursion of FMD into disease-free countries can have a devastating impact as was shown in the UK in 2001  and 2007 , or in Taiwan during 1997 .
FMD is caused by a non-enveloped picornavirus (FMDV: genus Aphthovirus) with icosahedral symmetry. The virion, approximately 30 nm diameter, contains a single-stranded positive-sense RNA genome of approximately 8500 nucleotides (nt) in length. It contains a single open reading frame which is flanked by 5′ and 3′ untranslated regions (UTRs) and encodes the four structural proteins which form the capsid [1A (also known as VP4); 1B (VP2); 1C (VP3) and 1D (VP1)], and ten non-structural proteins (L, 2A, 2B, 2C, 3A, 3B1-3, 3C, and 3D) (for reviews see [6, 7]). FMDV is a rapidly evolving virus classified into seven distinct serotypes, i.e. O, A, C, Asia 1, and Southern African Territories (SAT) 1, SAT 2 and SAT 3, which are supported by genetic classification based on the VP1-coding region. Most of our knowledge about the global distribution and molecular epidemiology of the virus is dependent upon analysis of this region which comprises approximately 8% of the FMDV genome . However, complete genome sequences of FMDV are required to fully understand viral determinants of pathogenicity, virulence, host range and evolution. Moreover, complete genome sequence analysis of FMDV isolates has been successfully used to trace the origin and the transmission pathways of the virus within an outbreak [4, 9–11].
During 2010–2011, incursions of the Mya-98 lineage of the Southeast Asia (SEA) topotype of serotype O (O/SEA/Mya-98) caused a series of high profile FMD outbreaks across five East Asian countries: the People’s Republic of China (PR China) including the Hong Kong Special Administrative Region (SAR), Japan, Mongolia, the Russian Federation (Russia) and the Republic of Korea (ROK; South Korea) [12–15]. A range of host species have been affected by these outbreaks including domesticated pigs, cattle and small ruminants, as well as evidence for infection in gazelles in Mongolia. Previous pandemic waves of FMD have affected many East Asian countries: during 1999–2002, the O/ME-SA/PanAsia lineage caused widespread outbreaks in PR China, ROK and Japan (in 1999–2000, 2000 and 2002 and 2000, respectively) prior to those in South Africa (2000) and Europe (2001) [3, 16]. During 2005–2007, serotype Asia 1 also spread throughout many countries in the region (PR China, Mongolia, Russia, North Korea); although it was not possible to determine the precise origin of these outbreaks, Southeast Asia was not implicated . In ROK and PR China the outbreaks due to O/SEA/Mya-98 were preceded by FMD outbreaks due to serotype A (A/ASIA/Sea-97 lineage) . Together, these recent events may be indicative of changing epidemiology of FMD in East Asia which may heighten risk for onward transmission to more distant countries including those that are FMD-free.
The aim of this study was to analyse the complete genomes of representative FMD viruses recovered from outbreaks during the pandemic of O/SEA/Mya-98 in East Asia and to compare them with sequences from viruses from Southeast Asia where this lineage is endemic . Furthermore, previously uncharacterised FMD outbreaks due to serotype O also occurred during 2011 in the Democratic People’s Republic of Korea (DRK; North Korea) and analysis of one of these samples are included in this report. This study investigates the origin and evolution of this emerging virus lineage.