Cell
ArticleHIV infection does not require endocytosis of its receptor, CD4
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2020, Current Opinion in PharmacologyVirus–Receptor Interactions: The Key to Cellular Invasion
2018, Journal of Molecular BiologyDistinct requirements for HIV-cell fusion and HIV-mediated cell-cell fusion
2015, Journal of Biological ChemistryCitation Excerpt :Although the mechanism of Env-mediated fusion is reasonably well understood (1–3), the sites of HIV-1 entry into cells remain controversial (4, 5). The widely held view that HIV-1 directly fuses with the plasma membrane (6–11) has been challenged by several studies showing pH-independent endocytic entry of this virus into different cell types, including primary macrophages (12–23). We have previously provided functional evidence supporting HIV-1 entry through endocytosis in adherent cells and CD4+ T cell lines (13).
Human Immunodeficiency Viruses
2014, Mandell, Douglas, and Bennett's Principles and Practice of Infectious DiseasesHIV entry: A game of hide-and-fuse?
2014, Current Opinion in VirologyCitation Excerpt :Direct HIV fusion with the PM has long been regarded as the only productive pathway. The following observations support this notion: (1) HIV Env is capable of mediating cell–cell fusion at neutral pH (e.g. [5]), and HIV particles can fuse two adjacent cells, a phenomenon referred to as ‘fusion from without’ [21]; (2) mutations in the cytoplasmic domains of CD4 or coreceptors that impair constitutive and ligand-mediated endocytosis of these proteins do not inhibit HIV infection [22–24]; (3) although HIV particles pseudotyped with the Vesicular Stomatitis Virus (VSV) G protein enter via endocytosis and are highly infectious, the fact that infection by these pseudoviruses no longer requires Nef and is less sensitive to mutations that alter the capsid stability [25–27] suggests distinct entry routes for HIV and VSV G pseudotypes; and (4) HIV, but not VSV G pseudoviruses, can infect resting CD4+ T cells [28,29•] (but see the next section for further discussion). HIV Env-mediated cell signaling and actin remodeling have been implicated in multiple steps of entry, from CD4/coreceptor clustering [30–34] to reverse transcription [35,36].
Mechanisms of enveloped virus entry by membrane fusion
2012, Comprehensive Biophysics