Sequencing and phylogenetic analysis of the coding region of six common rotavirus strains: Evidence for intragenogroup reassortment among co‐circulating G1P[8] and G2P[4] strains from the United States

The segmented genome of rotaviruses provides an opportunity for rotavirus strains to generate a large genetic diversity through reassortment; however, this mechanism is considered to play little role in the generation of mosaic gene constellations between Wa‐like and DS‐1‐like strains in genes other than the neutralization antigens. A pilot study was undertaken to analyze these two epidemiologically important strains at the genomic level in order to (i) identify intergenogroup reassortment and (ii) to make available additional reference genome sequences of G1P[8] and G2P[4] for future genomics analyses. The full or nearly complete coding region of all 11 genes for 3 G1P[8] (LB2719, LB2758, and LB2771) and 3 G2P[4] (LB2744, LB2764, and LB2772) strains isolated from children hospitalized with severe diarrhea in Long Beach, California, where these strains were circulating at comparable rates during 2005–2006 are described in this study. Based on the full‐genome classification system, all G1P[8] strains had a conserved genomic constellation: G1‐P[8]‐I1‐R1‐C1‐M1‐A1‐N1‐T1‐E1‐E1‐H1 and were mostly identical to the few Wa‐like strains whose genome sequences have already been determined. Similarly, the genome sequences of the 3 G2P[4] strains were highly conserved: G2‐P[4]‐I2‐R2‐C2‐M2‐A2‐N2‐T2‐E2‐E2‐H2 and displayed an overall lesser genetic divergence with reference DS‐1‐like strains. While intergenogroup reassortment was not seen between the G1P[8] and G2P[4] strains studied here, evidence for intragenogroup reassortment events was identified. Similar studies in the post‐rotavirus genomic era will help uncover whether intergenogroup reassortment affecting the backbone genes could play a significant role in any potential vaccine breakthrough events by evading immunity of vaccinated children. J. Med. Virol. 83:532–539, 2011. © 2011 Wiley‐Liss, Inc.