Figure 4.

The recruitment of the ESCRT cellular factors by L domains in HIV Pr55^Gag ensures viral particles release. The cellular factor angiomotin (AMOT) promotes the recruitment of the ubiquitin ligase NEDD4L at HIV-1 budding sites. The ESCRT machinery is then recruited by NEDD4 family, and this interaction seems to be related to the ubiquitination of viral structural proteins. The P(T/S)AP L domain of Pr55^Gag recruits the ESCRT-I factor TSG101 at viral assembly sites by direct binding to its ubiquitin E2 variant (UEV) domain, and the YPXnL motif recruits the ESCRT-III-associated factor ALIX by binding to its V domain. The ESCRT-III proteins drive the interaction with the VPS4 ATPase. This late-acting factor leads to membrane remodeling and its fission, and it drives the disassembling of the ESCRT-III filaments. The process ends with the release of the newly formed viral particle.