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. 2020 Aug 24;253(5):399–423. doi: 10.1007/s00232-020-00135-0

Fig. 3.

Fig. 3

Schematic depicting HIV life cycle within the host cells. The entry process begins with the binding of viral spike protein gp120 to CD4 receptors and CCR5 and CXCR4 co-receptors situated within the host lipid raft domains, followed by a conformational change that exposes the fusion peptide of gp41. Upon fusion, the virus releases its single-stranded RNA-genome along with its reverse transcriptases for the formation of viral DNA, followed by integration with the host DNA and replication leading to the release of m-RNA. In the cytosol, the structural and enzymatic viral proteins are expressed including Pr55Gag, which are critical for the viral assembly and budding. HIV RNA assembles at the inner leaflet of the cell membrane and form an immature HIV virus. The subdomains of Gag protein are involved at different stages of the budding process. The MA domain is anchored to the cell membrane via a myristate along with basic amino acids that preferentially interact with acidic lipids of the host raft domains. The capsid domain (CA) contains amino acids that promote Gag-Gag interactions (multimerization) that invaginate the membrane, initiating the budding process. The nucleocapsid domain (NC) binds to viral RNA that are packaged in the virus particle. Before release, viral proteases cleave Gag to form a mature virus. Upon maturation, the new virus buds out from the infected host cell along with a part of the host cell membrane as its own viral membrane