Human respiratory syncytial virus (HRSV) is the most common cause of serious acute lower respiratory tract disease among infants and young children, and is found mainly in late fall, winter, and spring in temperate zones of the world (6). Some 50% to 70% of infants experience infection in the first year of life, and virtually all are infected by 2 years of age (3). In a population-based birth cohort study, 1.1% of the cohort were admitted to the hospital within 12 months of birth with HRSV-induced bronchiolitis (14). The consequences of HRSV infection in children with underlying conditions, such as prematurity, cardiac and pulmonary disease, or immunosuppression, may include prolonged substantial illness and even death (18,38). Reinfections are very common throughout life (7,10,11,13).HRSV belongs to the family Paramyxoviridae and has a nonsegmented, negative-sense RNA genome of approximately 15,200 nucleotides (3). HRSV has been classified into antigenic subgroups A and B (HRSV-A and HRSV-B, respectively), initially on the basis of the reactivity of the virus with monoclonal antibodies directed against the attachment glycoprotein (G protein) (1,5,15,21) and now by genetic analyses (9,19,(31)(32)(33).The G protein is the most variable HRSV protein, with two hypervariable regions. Its C-terminal region (the second hypervariable region) accounts for strain-specific epitopes (2-4, 9, 16, 27, 29, 31). The molecular epidemiology and evolutionary patterns of the G protein have provided important information about the epidemiological features of HRSV. Some studies showed that several different genotypes cocirculated and some predominated in a community every year (23, 27). However, the relationship between strain diversity and the clinical and epidemiological features of HRSV has yet to be elucidated in detail.The subgroups have been subdivided further, into genotypes, by genetic analyses. HRSV-A is divided into seven genotypes (GA1 to -7) and HRSV-B into four genotypes (GB1 to -4) (3,8). An additional HRSV-A genotype, SAA1, has been proposed, as well as the new HRSV-B genotypes SAB1 to -3 (37). Another HRSV-B genotype includes the Buenos Aires (BA) type strain, which has a 60-nucleotide insertion in the second hypervariable region of the G protein and has been reported in Buenos Aires in 1999, as well as in other areas of the world (31,35,40). BA strains are further subdivided into six clusters (BA-I to BA-VI) (36).National surveillance of HRSV infection based on weekly reports from sentinel pediatric clinics throughout Japan began

Phylogenetic analysis of respiratory syncytial virus (RSV) group B genotype BA strains from the 2002-2003 to 2009-2010 seasons collected in Niigata, Japan, revealed four distinct clusters, designated new BA genotypes BA7, BA8, BA9, and BA10. These new genotypes were not associated with large outbreaks in the community.

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In tandem and diffuse coronary disease, iFR pullback predicted the physiological outcome of PCI with a high degree of accuracy. Compared with angiography alone, availability of iFR pullback altered revascularization procedural planning in nearly one-third of patients.

The guidewire recrossing point and the location of a stent link at the SB orifice had an influence on the ISA. KBD with optimal conditions under 3D-OCT guidance may reduce SB restenosis.