ICP47 is an iconic immune modulator encoded by HSV that hides infected cells from CD8+ T cells by inhibiting the presentation of peptides on MHC class I. The mechanism by which ICP47 exerts this function is by binding to the transporter associated with antigen processing (TAP), blocking peptide transport and loading onto MHC I. The first studies of ICP47 noted a marked species specificity with human but not mouse TAP being inhibited by this protein. Despite these seemingly absolute biochemical and in vitro observations, later work showed that ICP47 can contribute to HSV neurovirulence in mice. The use of mouse models remains a mainstay of HSV research in vivo, so we reexamined this controversy using a new set of ICP47 null viruses, a flank infection model and unique methods to quantify the effect of ICP47 on levels of antigen presentation. In a flank infection model using HSV KOS, deletion of ICP47 did not alter lesion development, or virus load, spread and reactivation. Likewise latency was unaffected by ICP47 deficiency as determined using a sensitive Cre-marking mouse model. By contrast, we were able to show that ICP47 does inhibit antigen presentation significantly on HSV-infected mouse cells using in vitro antigen presentation assay. Consistently, using mass spectrometry we found that more peptide sequences were presented on mouse cells infected with ICP47 mutant virus compared to those infected with wildtype virus. However, in mice the inhibition of antigen presentation was 44%, in comparison to human cells where presentation was reduced by 85%. In conclusion, this study shows that despite significant inhibition of antigen presentation in mouse cells, ICP47 is not an effective immune modulator in mice where HSV is confined to the peripheral nervous system.