Introduction of the template sequence mutation in vTR in the context of the viral genome and infection of MD-susceptible chickens with mutant virus (vAU5) resulted in complete absence of tumors and low-level viral replication in vivo (Fig. 4). Secondary mutation of the vTR stem-loop sequence (P6.1), abolishing the interaction of mutant vTR with TERT, restored virus-induced tumorigenesis (Fig. 6), thus showing that vTR-TERT interaction and functional telomerase activity is required for the anti-tumorigenic effects of the mutant template sequence in a viral background. Here, TERT is linked to infection.