New information about the mechanisms of varicella-zoster virus (VZV) pathog
enesis and the host response to the virus has improved our understanding of
the threat that VZV reactivation may pose after hematopoietic cell transpl
antation (HCT). Antiviral therapy compensates for some of the deficiencies
in VZV immunity in HCT recipients, and inactivated varicella vaccine may be
useful for the early reconstitution of adaptive immunity to VZV after HCT.