The molecular epidemiology of varicella zoster virus (VZV) has led to an understanding of virus evolution, spread, and pathogenesis. The availability of over 20 full length genomes has confirmed the existence of at least five virus clades and generated estimates of VZV evolution, with evidence of recombination both past and ongoing. Genotyping by restriction enzyme analysis (REA) and single nucleotide polymorphisms (SNP) has proven that the virus causing varicella is identical to that which later reactivates as zoster in an individual. Moreover, these methods have shown that reinfection, which is mostly asymptomatic, may also occur and the second virus may establish latency and reactivate. VZV is the only human herpesvirus that is spread by the respiratory route. Genotyping methods, together with epidemiological data and modeling, have provided insights into global differences in the transmission patterns of this ubiquitous virus.