Abstract
Background Assembly and release of HIV-1 particles occurs at the plasma membrane and is dependent on trafficking of Gag from sites of protein synthesis to sites of particle assembly. For example, the interaction of HIV-1 Gag with components of cellular trafficking pathways such as clathrin adaptor proteins (AP) 1 and 3 has been shown to be required for HIV-1 virion production [1,2]. This is likely to place a large burden on cellular trafficking pathways, but this has not previously been investigated. We addressed the questions of whether HIV-1 disrupts cellular protein trafficking and whether HIV-2 has the same effect.
Highlights
And release of HIV-1 particles occurs at the plasma membrane and is dependent on trafficking of Gag from sites of protein synthesis to sites of particle assembly
Both HIV-1 and HIV-2 Gag localised to endosomal compartments, a decrease in the proportion at the plasma membrane, and a reduction in virion release
HIV-2 has a disruptive effect on the endosomal pathway, and we observed that HIV-2 Gag accumulates in endosomal compartments
Summary
And release of HIV-1 particles occurs at the plasma membrane and is dependent on trafficking of Gag from sites of protein synthesis to sites of particle assembly. The interaction of HIV-1 Gag with components of cellular trafficking pathways such as clathrin adaptor proteins (AP) 1 and 3 has been shown to be required for HIV-1 virion production [1,2]. This is likely to place a large burden on cellular trafficking pathways, but this has not previously been investigated. We addressed the questions of whether HIV-1 disrupts cellular protein trafficking and whether HIV-2 has the same effect Both HIV-1 and HIV-2 Gag localised to endosomal compartments, a decrease in the proportion at the plasma membrane, and a reduction in virion release
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