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HIV-1 entry is the multi-step process by which the virus attaches to, fuses with, and penetrates host cells. The key steps are: binding of the viral envelope glycoprotein (Env, comprised of gp120/gp41 heterotrimers) to the CD4 receptor on the host cell surface; subsequent interaction with a chemokine coreceptor, usually CCR5 or CXCR4; and triggering of conformational changes in gp41 that result in fusion of viral and host cell membranes, releasing the viral core into the cytoplasm[1][3][4]. These molecular events are the targets of several classes of antiretroviral drugs. Entry inhibition is a highly validated therapeutic approach for HIV/AIDS[1][3].
Blocking Env interaction with CD4 or coreceptors\nInhibiting gp41-mediated membrane fusion\nPreventing conformational changes necessary for viral fusion and entry
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