Interestingly, the fact that HIV-1 ∆Vpu replication could reach levels similar to those of HIV-1-WT at late time points post infection at low dose suggests that over time BST2 antagonism by Vpu appears less imperative most likely because viral cell-to-cell transmission, a form of viral spread that is highly efficient [39,40] and perhaps less sensitive to BST 2 restriction [9,41], becomes the predominant form of viral propagation. Here, BST2 is linked to infection.