Indirect evidence suggesting that control of actin polymerization may be important for ZEBOV infection came from observations that: (i) internalized ZEBOV particles were in close proximity to actin bundles or filaments; (ii) inhibitors of PI3K, Akt and Rac1 all caused similar changes in F-actin characterized by loss of membrane ruffling and focal adhesions (data not shown); and (iii) agents that perturb actin dynamics significantly inhibit EVP entry [26]. Here, AKT1 is linked to infection.