Immune responses to varicella zoster virus and effective vaccines

Varicella zoster virus (VZV) causes two distinct diseases, varicella (chickenpox) during primary infection, and herpes zoster (shingles) resulting from reactivation. The purpose of this review is to summarize the present understanding of VZV and the associated immune response, as well as to discuss available vaccines. VZV infection induces both innate and adaptive immune responses, especially an antigen-specific adaptive immune response, which activates humoral immunity and cell-mediated immunity (CMI). Reactivation of VZV can occur when the CMI of latent VZV is reduced, leading to herpes zoster. After VZV infection, natural killer (NK) cells modulate antigen presentation and the production of IFN-γ, an important activator of macrophages. IFN-γ is produced by NK cells and CD4 Th1/CD8 cytotoxic T lymphocytes. The T cell-mediated immune response is an important factor influencing VZV reactivation and herpes zoster, with herpes zoster being associated with reduced levels of VZV-specific T cells. Since the VZV-specific T cell population gradually declines with age, herpes zoster particularly affects the elderly. There are two types of zoster vaccines: live-attenuated and recombinant subunit. However, recombinant vaccines generally have poor immunogenicity when admini-stered alone and require an adjuvant. Therefore, effective adjuvants are needed that especially promote cell-mediated immune responses. Various adjuvants have been developed, many of which enhance T cell immunity more than antibody-based humoral immunity. The information presented in this review may serve as a reference for future VZV immunology studies.