INTRODUCTION Rotavirus A (RVA) is a major cause of gastroenteritis in infants and young children worldwide. In 2016, RVA caused 128,500 deaths in children under 5 years of age globally (1). Although most of these deaths occurred in developing countries, RVA imposes a huge burden even in developed countries, including Japan (2-4). Live attenuated RVA vaccines were introduced in Japan in 2011 (Rotarix ® , GlaxoSmithKline Biologicals, Rixensart, Belgium) and in 2012 (RotaTeq ® , Merck & Co., Inc., Kenilworth, NJ, USA), and while RVA vaccines have proven to be effective (5,6), the selective pressure of a vaccine may induce an epidemic strain shift (7-10). The RVA genome contains 11 gene segments of double-stranded RNA that encode six structural (VPs) and six nonstructural proteins (NSPs) (11). To classify RVAs, a specific genotype is assigned to each of the 11 genome segments, according to predefined nucleotide sequence identity cutoff values (12-14). The classification system denotes the VP7-VP4-VP6-VP1-VP2-VP3-NSP1-NSP2-NSP3-NSP4-NSP5 6 genes of an RVA strain as a descriptor Gx-P[x]-Ix-Rx-Cx-Mx-Ax-Nx-Tx-Ex-Hx (x indicating genotype number),