162: 53C56. limited within the small area. Inadequate environmental temperatures Glucokinase activator 1 for vector transmission in late autumn might have limited the virus spread to a wider region. The reemergence of Ibaraki disease showed us the importance of continuous vaccination to prevent economic losses. of the family [3, 5]. The EHDV particle is composed of seven structural proteins and 10-segmented, double-stranded RNA genomes Glucokinase activator 1 [8, 15]. The major outer coat protein, VP2, is usually encoded by genome segment 2 and is highly variable among the eight serotypes of EHDV. The specificity of the conversation of VP2 with neutralization antibodies is usually thought to be a major determinant of the virus serotype [3]. It was reported that VP2 of IBAV has 96.8% and 73.6% amino acid (aa) identities with those of Australian and Canadian strains of EHDV serotype 2, respectively, but less than 68.5% aa identity with that of other EHDV serotypes [3]. In contrast, segment 3 encodes the major core protein, VP3, and is highly conserved among EHDV isolates and is used as a target for EHDV group-specific diagnostics [21]. However, a small variation in the core protein is available for typing EHDV isolates based on their geographic origin [4]. IBAV isolates are sorted into an eastern topotype with Australian EHDV strains. As are the other EHDV strains, IBAV is regarded as an arthropod-borne virus (arbovirus) transmitted by biting midges [24, 32]. Therefore, the seasonal activity and geographic distribution of vectors potentially affect the epidemic period and range of Ibaraki disease. The ability of IBAV to overwinter in Japan is usually unlikely, and the virus was presumably introduced from lower latitudes with the infected midges carried on seasonal winds in the summer [32]. Ibaraki disease was first Glucokinase activator 1 recognized in Japan in 1959 as an acute febrile disease resembling bluetongue [23]. During the 1959C60 Ibaraki disease epidemic, 43,793 cases and 4,298 deaths were reported. Smaller outbreaks occurred in southern Japan in 1982, FGF1 1987 and 1997C98 [9, 12, 28,29,30]. In addition to the common Ibaraki disease manifestations, more than 1,000 cases of abortion and still birth were observed in the infected pregnant cows in the 1997C98 outbreak [20]. The virus isolated from the aborted fetuses was serologically related to IBAV but genetically distinct from the previous IBAV isolates, and was thought to be an IBAV variant within EHDV serotype 2 [20, 22]. The prevalence of EHDV serotype 1 was also reported in Japan, but no association between that virus and cattle morbidity has been detected [17]. Kagoshima Prefecture is located at the southern end of Japans mainland and includes islands spreading 500 km further to the southwest. Due to its geographic location, the prefecture has been thought of as one of the gates for arbovirus incursions [10, 32]. In October 2013, two cows with foamy salivation and difficulty swallowing were found in the northwestern a part of Kagoshima Prefecture and were suspected to be cases of Ibaraki disease. We report here the identification of a causative agent of the disease, and we describe the epidemiological aspects based on sentinel surveillance in Kagoshima Prefecture. MATERIALS AND METHODS for 10 min. The blood cells were washed three times with phosphate-buffered saline (PBS) and resuspended in PBS. Serum samples were obtained from the above-mentioned cattle at the same time and 2 weeks later. In June 2013, 120 calves that had not experienced summer were selected from all over Kagoshima Prefecture for sentinel arbovirus surveillance. Heparinized blood and serum samplings were obtained from the calves in June, August, September and November. The processed plasmas and blood cells were kept at ?80C until the virus isolation and viral genome.