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Background Cellular entry of HIV-1 occurs through fusion at the plasma membrane (PM) or via endocytosis. PM fusion, resulting in deposit of nucleocapsid into the cytoplasm, typically establishes productive infection. In contrast, entry through endocytosis results in either lysosomal degredation, or productive infection through endosomal membrane fusion. While viral entry and permissivity are known to differ between host cells, the influence of these differences on antibody-mediate neutralization is unknown. Here we explore the relationships between HIV-1 entry, neutralization sensitivity, and the mechanisms by which antibodies act.

The impact of differences in viral entry and trafficking on the mechanism of HIV-1 neutralization