The VP1 BC and HI loops receive the VLDL-R molecule among some minor group HRV strains [12, 46, 47] . The comparative reduction in size of protrusions along the 5-fold axis, resulting from deletions in the BC, DE and HI loops of the HRV-QPM VP1, together with structure-altering deletions and substitutions affecting some antigenic sites previously identified from a minor group strain (HRV-2), particularly site A, lead us to propose that HRV A2 viruses are unlikely to behave as members of the minor group. Mapping the known ICAM-1 contact sites onto the predicted HRV-QPM structure revealed that most of the footprint was retained in structure by HRV-QPM, although it differed in sequence compared to other major group strains. SimPlot data revealed that sequence variation was not uncommon among strains within the major groups. Two small a-helices predicted to form in the HRV-QPM VP1 and VP3 footprints may disrupt receptor binding but since ICAM-1 is predicted to attach at differing angles in different HRV strains [8] , it may be suitably flexible to overcome such obstacles. Although NImIA and NImIB, first identified in a major group virus (HRV-14), were affected by the deletions in VP1, additional support for HRV-QPM belonging to the major HRV group came from structural similarities in the NImII (VP2) and NImIII (VP3). Amino acid substitutions occurred at these sites (ERG and GRT respectively) rather than insertions or deletions. These variations may result in distinct immunogenicity.