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Cell surface receptors for viral entry are a diverse group of host plasma membrane proteins, glycoproteins, or lipids that viruses exploit to attach to and enter host cells[1][4][5][7]. These receptors determine viral host range, tissue tropism, and the efficiency of infection. Individual viral families often use characteristic receptors; for example, coronaviruses (like SARS-CoV-2) use angiotensin-converting enzyme 2 (ACE2), HIV uses CD4 with CCR5 or CXCR4, and filoviruses may use NPC1. These receptors may function alone or as part of multi-component entry complexes, sometimes requiring coreceptors or attachment factors. They are prominent therapeutic targets: antibodies or small molecules that block virus-receptor interactions can prevent viral entry, although blocking host proteins raises toxicity and selectivity challenges[1][6]. "Cell surface receptors for viral entry" is a collective term and not a canonical target name, so it is not specific enough for direct drug targeting or unambiguous indexing in therapeutic databases. Key Points: - This is not a single molecule, but an umbrella category for a large set of proteins (e.g., ACE2, CD4, AXL, NPC1) used variably by different viruses[1][6]. - The target name is too generic; for structured data, each specific receptor should be named (e.g., "Angiotensin-converting enzyme 2" for ACE2). - The importance of these receptors in viral infection and therapy makes each a critical target for drug and vaccine development, but drug selectivity and potential interference with normal host processes are a concern[6][9]. For precise structured information, identification of the exact receptor (e.g., ACE2, CD4) in context is essential.
Blockade of virus-receptor interaction, Competitive inhibition, Receptor mimetic, Antibody-mediated receptor blockade
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