Many viruses are able to manipulate the host cell environment to benefit viral replication, with modulation of the cell cycle to a favourable phase a common strategy. Using the Murine norovirus (MNV-1) model for caliciviruses we identified changes to the host cell cycle induced by viral infection. Microarray analysis of MNV-1 infected RAW-Blue cells showed changes in cell cycle regulators that were confirmed by Western blot analysis. The expression of the cell cycle regulator cyclin A was strongly inhibited by viral replication, indicating cell cycle effects at the G1/S checkpoint. Cell cycle analysis confirmed that MNV-1 infection caused a prolonging of the G1 phase and an accumulation of cells in the G0/G1 phase caused by a reduction in cell cycle progression through the G1/S restriction point. MNV-1 replication was compared in populations of cells synchronised into specific cell cycle phases or in asynchronously growing cells. Cells actively progressing through the G1 phase had a 2-fold or higher increase in virus progeny and capsid protein expression over cells in other phases of the cell cycle or in unsynchronised populations. Furthermore, screening of MNV-1 ORF1 encoded proteins has indicated a candidate protein responsible for the G1 cell cycle arrest. These findings suggest that MNV-1 infection leads to prolonging of the G1 phase and a reduction in S phase entry in host cells, establishing favourable conditions for viral protein production and viral replication. There is limited information on the interactions between noroviruses and the cell cycle and this observation of increased replication in the G1 phase may be representative of other members of the Caliciviridae.