Rotaviruses evolve through the accumulation of point mutations (drift) and through reassortment of genes (shift) during the dual infection of a single cell. The accumulation of point mutations at antigenic sites or primer binding sites render immunological and molecular methods of serotyping and genotyping, respectively, redundant. Monoclonal antibodies to the variant virus antigens or redesigned oligonucleotide primers complementary to the primer-binding site need to be generated.