Viruses are by definition fully dependent on the cellular translation machinery, and develop diverse mechanisms to co-opt it for their own benefit. Unlike many viruses, HCMV does not suppress the host translation machinery, and the extent to which translation machinery contributes to the overall pattern of viral replication and pathogenesis remained elusive. By simultaneously examining the changes in transcription and translation along HCMV infection, using ribosome profiling and RNA-seq, we uncover diverse and dynamic translational regulation for subsets of host genes. Although ribosome profiling provides precise and quantitative analysis of genes that are translationally regulated, our molecular understanding of this type of regulation is still at its infancy. We develop approaches that will allow better understanding of this regulation.