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HIV entry refers to the process by which the Human Immunodeficiency Virus (HIV) attaches to and penetrates host cells, initiating infection. This is a critical early step in the viral life cycle and a major determinant of viral tropism, transmission, and pathogenesis. The process involves sequential interactions between viral envelope proteins (gp120 and gp41) and host cell receptors (CD4 and co-receptors CCR5 or CXCR4). Therapeutic targeting of HIV entry is achieved using entry inhibitors like attachment inhibitors, CCR5 antagonists, and fusion inhibitors.
Varies depending on the specific entry inhibitor class: - Pre‐attachment inhibitors (e.g., Fostemsavir): Blocks gp120–CD4 binding - Post‐attachment inhibitors (e.g., Ibalizumab): Binds CD4 away from binding site; prevents conformational changes - CCR5 antagonists (e.g., Maraviroc): Blocks CCR5 co‐receptor - Fusion inhibitors (e.g., Enfuvirtide): Prevents HR1/HR2 association in gp41; blocks membrane fusion
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