Figure 4.

Exocytosis vesicles participate in herpesvirus exit. (A) The accumulation of herpesvirus capsids in the cytoplasm has been shown to be assisted by VAPB host proteins. (B) The HSV-1 Us9 protein interacts with capsids in the endoplasmic reticulum (ER), the Golgi apparatus and the cytosol in order to promote the anterograde transport of viral components through microtubules. Us3 protein has also been shown to stabilize and activate microtubules and CLASP complexes to promote vesicle transport. The interactions of viral gD with host M6P and its receptors promote the export of virus-containing late endosomes. On the other hand, viral proteins have been shown to co-localize with CD63 or CD63 and MHC-II, suggesting a potential immune-modulatory role for late endosomal trafficking. (C) VZV has been reported to use M6P and its receptors to promote viral export. Additionally, this virus appears to be exocytosed in single-membrane vesicles from the autophagosomal pathway, which contain LC-3 and Rab II. (D) EBV shuttles LPMI- and miRNA-containing vesicles derived in exosomal traffic modulation. (E) Exit of HHV-6 occurs through the exosomal pathway, using multivesicular bodies (MVBs). (F) Finally, KSHV recycles clathrin-coated endosomal vesicles, used during cell entry, for viral exit using the viral protein ORF65.