Our targeting of udg, rather than another essential MVA gene, was based partly on initial studies by Holzer and co-workers that demonstrated the feasibility of trans-complementation of a udg-deletion in vaccinia virus, and that a udg-deletion mutant of vaccinia virus, which also expressed the prM and E structural proteins of tick-borne encephalitis virus (TBE), was better able to protect mice against lethal TBE challenge than was a replication-competent VV recombinant [39], [52], [58]. The gene discussed is UNG; the disease is tick-borne encephalitis.