We find that internal Atractylenolide-II acidification has no influence on fusion kinetics, but that a drop in internal pH nonetheless generally precedes fusion-pore formation. The results support a transporter model, in which the channel histidines participate in moving protons down a concentration gradient. Parallel measurements of kinetics of internal virion acidification and membrane pore-formation allow direct comparisons of the relative timing of the two processes. The onset of internal virion acidification generally precedes that of pore formation, but the latter does not require acidification to proceed at its normal rate. The kinetics of pore formation were unchanged in the Tripdiolide presence of 10 mM rimantadine, which blocked internal virion acidification. Thus, there appears to be no direct molecular signal linking acidification to pore formation. Nonetheless, because fusion with the endosomal membrane will equilibrate the virion with that of the cytosol, release of nucleocapsid from M1 requires that proton transport be rapid enough to reduce the internal pH before a fusion pore opens. Our results show that this relationship holds. We do observe, however, a small overlap in the distribution of pore-formation onset times with that of acidification onset times. During cell entry, a corresponding fraction of early pore-formation events might include non-productive infections, if pore formation were to occur before an adequate drop in internal pH. Because of the relatively small size of our probe, our observations leave open the possibility that internal virion acidification could influence the transition from initial opening of a small fusion pore to widening of that pore into a channel large enough for genome translocation. In addition to showing the mutual independence of membrane fusion and internal virion acidification, the methods described here provide a format for studying specific inhibition of either of these low-pH-induced processes, both of which are essential for productive viral entry. Macroscopic and histological observations in ASD include findings of ileo-colonic lymphoid nodular hyperplasia, enterocolitis, gastritis, and esophagitis.