The term ‘endocytosis’ includes at least four mechanisms: phagocytosis, macropinocytosis, clathrin mediated endocytosis, and caveolin mediated endocytosis, which differ in several properties such as vesicular size, markers and regulation. Different viruses use cellular endocytic mechanisms to enter and infect cells with the clathrin mediated pathway being the most commonly observed uptake pathway. Once HIV is internalized, virus particles can follow different pathways: they can be secreted (as in the case of transcytosis) or degraded, or they can fuse with vesicular membranes to inject the viral core into the cytoplasm and initiate the viral infection cycle. However, the exact contribution of endocytic pathways to the infection of CD4+ T lymphocytes and to HIV pathogenesis in vivo is mostly unknown, and the mechanisms governing endocytosis also remain unclear. This paper discusses recent developments in the study of HIV entry and the different experimental approaches that have caused the role of endocytic pathways in HIV infection to be revisited, with the aim of updating and formulating new perspectives in the field of HIV entry.
Endocytosis of HIV: anything goes. (2010) Trends Microbiol. 18(12): 543-551
The major pathway for HIV internalization in CD4+ T cells has been thought to be the direct fusion of virus and cell membranes, because the cell surface is the point of entry of infectious particles. However, the exact contribution of endocytic pathways to the infection of CD4+ T lymphocytes is unknown, and the mechanisms involved in endocytosis of HIV particles are unclear. Recent evidence suggests that endocytosis of cell-free and cell-associated virus particles could lead to effective virus entry and productive infections. Such observations have, in turn, spurred a debate on the relevance of endosomal entry as a mechanism of escape from the immune system and HIV entry inhibitors. In this paper, we review the endocytosis of HIV and discuss its role in HIV infection and pathogenesis.