V aricella-zoster virus (VZV) causes varicella by primary infection and herpes zoster by reactivation of the latent virus in the sensory ganglia of infected individuals. After primary infection, the immune response comprises VZV-specific antibody and T cell-mediated immunity (CMI), which are important for recovery from varicella. T cell responses are necessary to control latent VZV in the sensory ganglia. A lack or a declining level of CMI to VZV has been associated with a higher risk of development of herpes zoster (1).A varicella vaccine consisting of live, attenuated strain OKA (vOKA) has been developed in Japan and licensed for mass vaccination in Japan, South Korea, the United States, and several European countries or recommended for only selected groups of the population in other countries (2, 3). To prevent herpes zoster, a zoster vaccine containing 14 times as many PFU of vOKA than the varicella vaccine was developed and licensed for the vaccination of immunocompetent subjects older than 60 years in the United States in 2006 (4). Varicella and zoster vaccines are administered by the subcutaneous (s.c.) route. However, vaccination of immunocompromised individuals with live VZV vaccines can be problematic and different strategies for safe immunization need to be explored (5).Several clinical studies have indicated that the use of a heatinactivated VZV vaccine is an alternative mode of immunization of immunocompromised individuals. Triple vaccination of bone marrow transplant patients with a heat-inactivated varicella vaccine administered s.c. decreased the severity of herpes zoster (6) and four s.c. doses of a heat-inactivated zoster vaccine proved safe and immunogenic in patients with tumor malignancy, HIV-infected individuals, or hematopoietic stem cell transplant recipients (7). When healthy elderly subjects were immunized s.c. with a single dose of either live or heat-inactivated varicella vaccine, there were no differences in antibody responses or IFN-␥ production by peripheral blood mononuclear cells (8). These data indicated that a heat-inactivated VZV vaccine might be useful in preventing herpes zoster. However, protection against herpes zoster following immunization with either a live or heat-inactivated vaccine is not optimal and a more potent antigenic stimulus is needed to improve the efficacy of the vaccine in high-risk patients (9).The skin is a highly immunogenic organ (10). Noninvasive, needle-free liquid jet injection of liquid or powder into the skin has been used in clinical trials for immunization against viral infections (11-13). The barrier structure and thickness of the stratum corneum, the outermost layer of the skin, are similar in guinea pigs and humans (18.6 and 18.2 m, respectively) (14), and thus, the i.d. route of immunization and the effectiveness of a potential i.d. delivery device for humans can be tested in guinea pigs. Moreover, the parental OKA strain is attenuated in human