Many viruses, including murine norovirus (MNV), are able to manipulate the host cell cycle to induce a beneficial replication environment. Recently it has been shown that during an MNV infection viral protein genome-linked (VPg) delays progression of cells through the gap 1 (G1)/synthesis (S) transition of the cell cycle. Although all viruses in the Caliciviridae family encode a VPg protein it is unknown if the G1/S arrest induced by MNV VPg is conserved. Cell cycle analysis of asynchronous RAW-Blue cells transfected with VPg from norovirus genogroups I, II or IV revealed that 80 % of cells were in G0/G1 phase compared to 60 % of mock-transfected cells. A corresponding decrease in the percentage of cells in S phase was observed indicating that, similar to MNV VPg, these proteins are able to delay G1/S transition. When the search was expanded to include viruses from the wider Caliciviridae family VPg from rabbit haemorrhagic disease virus and human sapovirus showed a G1/S delay. In contrast transfection of VPg RNA from a GIII norovirus, feline calicivirus and newbury agent-1 virus were unable to delay the host cell cycle in murine RAW-Blue cells, suggesting conservation of a G1/S delay within some members of the Caliciviridae family.