HIV-1 entry

HIV-1 entry is the multi-step biological process by which the Human Immunodeficiency Virus type 1 (HIV-1) attaches to and penetrates a host cell, primarily CD4+ T lymphocytes and macrophages [11]. This sequence begins with the binding of the viral envelope glycoprotein gp120 to the host cell surface receptor CD4, which induces conformational changes in the viral protein [10]. These changes allow gp120 to interact with a co-receptor, typically the chemokine receptors CCR5 or CXCR4 [11]. Co-receptor binding triggers further structural rearrangements in the transmembrane subunit gp41, leading to the fusion of the viral and host cell membranes and the subsequent release of the viral capsid into the cytoplasm [10]. Pharmacological intervention in this process, known as entry inhibition, utilizes various drug classes including attachment inhibitors, post-attachment inhibitors, co-receptor antagonists, and fusion inhibitors [6]. These therapies are particularly valuable for treatment-experienced patients with multi-drug resistant HIV-1, though their use requires careful monitoring of viral tropism and potential safety concerns such as hepatotoxicity or injection site reactions [12].

Other names

HIV-1 fusionHIV-1 attachmentHIV-1 penetrationHIV-1 entry process

Inhibition of viral entry into host cells by blocking attachment to CD4, preventing co-receptor (CCR5/CXCR4) binding, or disrupting gp41-mediated membrane fusion.