The viral mitochondria-localized inhibitor of apoptosis (vMIA), encoded by the UL37 gene of
human cytomegalovirus, inhibits apoptosis-associated mitochondrial membrane
permeabilization by a mechanism different from that of Bcl-2. Here we show that vMIA
induces several changes in Bax that resemble those found in apoptotic cells yet take place
in unstimulated, non-apoptotic vMIA-expressing cells. These changes include the
constitutive localization of Bax at mitochondria, where it associates tightly with the …