Investigations of the pathogenesis of Varicella zoster virus infection in the SCIDhu mouse model.

Abstract

Varicella zoster virus (VZV) is a medically important human herpesvirus that causes varicella, establishes latency in sensory ganglia and may reactivate to cause herpes zoster in healthy and immunocompromised patients. Experiments in the severe combined immunodeficiency (SCID) mouse model have provided new insights about VZV pathogenesis. In addition, the evaluation of VZV recombinant viruses, with targeted mutations of viral genes or their promoters in SCIDhu skin, T-cell and dorsal root ganglia xenografts, has the potential to identify options for the design of a recombinant 'second-generation' VZV vaccine. This would be characterized by the retention of infectivity in skin combined with a restricted tropism for T-cells and neurons within sensory ganglia.