This conclusion is based on a number of observations, including; (1) although a low endosomal pH was shown to be essential for infection, the kinetics of BTV-1 delivery to acidic compartments was slower than expected for uptake by the clathrin pathway [53]; (2) during entry, BTV-1 did not co-localise with transferrin, a commonly used marker for CME; and (3) cell-entry and infection was not inhibited by expression of three different DN inhibitors of CME (AP180C, DN-Eps15 and DN-dynamin-2). Here, EPS15 is linked to infection.