Thus far, the protein composition of eight different herpesvirions has been studied by mass spectrometry. These studies include the alphaherpesvirinae herpes simplex virus type 1 (HSV-1) and pseudorabies virus (PRV; Loret et al., 2008; Kramer et al., 2011) , the betaherpesvirinae human and murine cytomegaloviruses (HCMV and MCMV, respectively; Kattenhorn et al., 2004; Varnum et al., 2004) and the gammaherpesvirinae Kaposi sarcoma herpesvirus (KSHV), gamma herpesvirus 68 (γHV68), Epstein-Barr virus (EBV), and Alcelaphine (Bortz et al., 2003; Johannsen et al., 2004; Bechtel et al., 2005; Zhu et al., 2005; Dry et al., 2008) . Interestingly, host proteins were detected in all herpesvirions analyzed so far, as summarized in Table 1 . For instance, our laboratory previously reported the protein composition of mature extracellular HSV-1 viral particles and identified as many as 49 cellular proteins (Loret et al., 2008) . Similarly, studies focusing on PRV and EBV reported up to 48 and 43 cellular proteins, respectively (Johannsen et al., 2004; Kramer et al., 2011) . Meanwhile, Varnum et al. (2004) found as many as 70 different host proteins in extracellular HCMV virions. While fewer cellular proteins were reported for other viral particles, it is clear that herpesviruses can potentially incorporate many proteins from its host. Moreover, of the 173 different proteins detected in herpesvirions, nine protein groups are present in at least four distinct herpesvirions. This includes 14-3-3, actin, annexins, cofilin, translation factors, GAPDH, heat shock proteins, pyruvate kinase M2, and various Rab GTPases. These results indicate that, first of all, it is common for herpesviruses to incorporate cellular proteins into their viral particles and, secondly, that www.frontiersin.org ? different viruses share similar host proteins. Most excitingly, it also suggests that these host proteins may play common roles throughout the herpesviral family. This defines an interesting and novel set of host-pathogen interactions taking place within the virus itself, rather than the cell. It is tempting to speculate that some viruses might have a higher capacity to steal cellular proteins because of their size and symmetry. Herpesviruses are indeed large viruses containing a layer called the tegument between their capsids and envelopes that could accommodate non-viral proteins. Though some host proteins may randomly be incorporated into virions, others may rather be selected to insure the optimal replication of the viruses that carry them.