medRxiv : the preprint server for health sciences · 2026
Experimental model of VZV reactivation reveals vaccine-induced mechanisms of protection against herpes zoster.
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Johnson Michael J, Vu Thao, Ford Emily S, Jing Lichen, Jordan Kimberly, Brown Mariah, Li Shaobing, Schedin Troy, Crotteau Megan, Canniff Jennifer, Bennett Ashlynn, Weaver Neil, Laing Kerry J, Frietze Seth, Koelle David M, Levin Myron J, Weinberg Adriana
Аннотация
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.