Some models propose that the ESCRTs bend the membrane, while others suggest that the ESCRTs are required during the split, providing the force for the cutting process. HIV can control ESCRTs to separate the bud from the cell, but where and how they are involved is still not fully understood. Cells usually use ESCRTs to cut membrane-bound compartments during cell division. These released virus particles are now able to infect other cells.īoth assembling and budding of the virus particles requires the help of specific cell proteins called ESCRTs. Gag aggregates inside of the host cell membrane, which then begins to bulge outwards forming a spherical bud that subsequently pinches off. The shell of HIV consists of thousands of copies of a protein called Gag, which helps to release the viruses. As the new viruses leave the cell, they wrap themselves in the membrane of their host cell. Once inside the cell, many viruses, including the HIV virus, hijack the cell’s genetic material to produce more HIV particles and release them back into the surroundings. Viruses need to be able to enter and leave the cells of their hosts to multiply and spread infections. This mechanistic insight is likely relevant for other ESCRT-dependent scission processes including cell division, endosome tubulation, multivesicular body and nuclear envelope formation, and secretion of exosomes and ectosomes. If scission does not occur within minutes of ESCRT departure, ESCRT-IIIs and VPS4 are recruited again. ESCRT-IIIs may pull the neck into a narrower form but must leave to allow scission. These observations suggest that ESCRT-IIIs are recruited by a combination of membrane curvature and the late domains of the HIV-1 Gag protein. By imaging single assembling viral-like particles of HIV-1, we observed that ESCRT-IIIs and the ATPase VPS4 arrive after most of the virion membrane is bent, linger for tens of seconds, and depart ~20 s before scission. Some viruses appropriate ESCRT-IIIs for their release. The Endosomal Sorting Complexes Required for Transport III (ESCRT-III) proteins are critical for cellular membrane scission processes with topologies inverted relative to clathrin-mediated endocytosis.
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