We investigated the functional relevance of the DS1C/A substitution as compared to wild-type DS1 C/EBP site, in the presence and absence of IFNβ, and whether such antiviral responses could explain why this genotype is undetectable in the brain early in infection (10–21 days p.i.)but emerges as a predominant genotype late in disease (42–84 days p.i.)when innate immune responses can no longer control virus replication [1]. The gene discussed is IFNB1; the disease is infection.