VV F1L has been shown to inhibit the mitochondrial pathway of apoptosis by replacing Mcl-126 and interacts with the isolated BH3 domains of Bim, Bax and Bak,23 which are bound in the canonical Bcl-2-binding groove.22 Furthermore, an F1L-deficient VV potently causes Bak/Bax-mediated apoptosis.15, 27 Functionally, VV F1L appears to rely primarily on neutralization of Bim in the context of a viral infection.22 Given the close similarity between VAR and VV, VAR may also rely on inhibition of host cell apoptosis for successful infection and proliferation. This evidence concerns the gene BAX and infection.