Experimental model of VZV reactivation reveals vaccine-induced mechanisms of protection against herpes zoster
Johnson, M. J.; Vu, T.; Ford, E. S.; Jing, L.; Jordan, K.; Brown, M.; Li, S.; Schedin, T.; Crotteau, M.; Canniff, J.; Bennett, A.; Weaver, N.; Laing, K. J.; Frietze, S.; Koelle, D. M.; Levin, M. J.; Weinberg, A.
Show abstract
Herpes zoster (HZ), caused by varicella zoster virus (VZV) reactivation, is common in older adults with declining cell-mediated immune protection. A modestly efficacious live attenuated (ZVL) and a highly efficacious recombinant adjuvanted (RZV) zoster vaccine protect against HZ. To uncover the mechanism(s) associated with the superior efficacy of RZV, we developed a controlled human infection model consisting of intradermal administration of attenuated vOka VZV to older adults previously vaccinated with RZV or ZVL. Infiltration of VZV-specific CD4+ and CD8+ T cell clonotypes at the infection site was quicker and higher in RZV than ZVL recipients [≥]5 years post-immunization due to the persistence of RZV-induced gE-reactive CD4+ and CD8+ T cell clonotypes in blood. High CD4+ cytotoxic T lymphocyte frequencies in blood on Day 1 post-inoculation predicted control of VZV replication. Persistence of circulating RZV-induced CD4+ and CD8+ CTL and rapid migration to sites of VZV replication are potential mechanisms underlying durable protection against HZ.
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