Models of HCMV entry pathways.

Abstract

<p><b>A–C). </b>HCMV TR, AD169 and TB40 are all taken up by dynamin-dependent endocytosis. If cells are induced to express increased PDGFRα, virus particles can fuse with endosomes by a low pH-independent mechanism, so that capsids enter the cytoplasm and can initiate infection after moving to nuclear pores. Without increased PDGFRα virus particles are degraded, presumably following delivery to lysosomes. <b>D–F</b>). Wild type HCMV TR particles which contain gH/gL/UL128–131 can also be taken up by macropinocytosis into endosomes. There is low pH-dependent fusion with endosomal membranes delivering capsids into the cytoplasm. It remains possible that AD169 and TB40 are also taken up by macropinocytosis but cannot exit endosomes derived from this process.</p