The overall picture that several important cellular functions might be modulated by the host proteins incorporated into viral particles is intriguing. This clever strategy is consistent with the parasitic nature of all viruses, including herpesviruses, which would presumably gain some replication advantage from stealing cellular modulators rather than coding for them in their own genomes. The most critical question is the benefit for the viruses to incorporate these cellular proteins in their assembled particles, particularly since these proteins also exist in the cells. While this is open to discussion, one possibility is that some of the incorporated cellular proteins may be remnants of the final capsid envelopment process. Alternatively, this may allow the prompt action of some of these proteins immediately upon viral entry. This could jumpstart the expression and/or duplication of the viral genome, as it is the case for the herpesviral VHS, VP16, ICP0, and ICP4 proteins that are present in virions (Lam et al., 1996; Everett, 2000; Halford and Schaffer, 2001; Ellison et al., 2005; Hancock et al., 2006; Loret et al., 2008; Sarma et al., 2008; Loret and Lippe, 2012) . Other early potential sites of action are the process of viral entry itself, intracellular capsid transport, import of the viral genome through the nuclear pore or immune modulation, all common steps among herpesviruses. Whatever the case might be, the question remains as to why the cellular pool of these proteins would not suffice. Several options may be considered. First, it may be that the virions incorporate specific isoforms, splice variants or post-translationally modified proteins that could have properties or functions distinct than their cellular counterparts. Second, the incorporation of a host protein from one cell type might permit the infection of a different cell type that does not express such protein. For example, alpha herpesviruses initially infect mucosal cells and could acquire host proteins that are beneficial to infect dormant neuronal cells. Finally, the host proteins might be in complex with viral proteins and it is those complexes that are active to promote the infection. These possibilities are of course speculative at this point and need to be explored.