While some studies suggest a greater antiviral role of type II IFNs (IFNγ) over type I IFNs (IFNα/β) against VZV in vitro [108], observations from patients with VZV CNS infection, pneumonitis or disseminated skin eruption/zoster in the context of defective Type I or Type II IFN pathways provide more indirect evidence of important non-redundant roles of both Type I and type II IFNs in protecting against VZV reactivation in humans [101,102,109,110]. This evidence concerns the gene IFNA1 and pneumonitis.