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An "influenza virus-infected cell" refers to any host cell, typically a respiratory epithelial cell, that has internalized and is supporting the replication of influenza virus. These cells constitute the primary site for viral genome replication, transcription, protein synthesis, and assembly of progeny virions. Infection triggers a cascade of host responses, including the production of interferons, chemokines, and other cytokines that activate the immune response[7][2]. While they can be useful in drug screening or as a means of describing the context of antiviral action, "influenza virus-infected cell" is not a specific molecule, protein, or receptor, and thus is not suitable as a classical therapeutic molecular target.
Antivirals inhibit viral proteins (e.g., neuraminidase, M2 ion channel), block viral replication, or enhance host immunity within infected cells[4][8][2]. Novel agents may induce or modulate the innate immune response (e.g., interferon inducers), or inhibit host cell functions required for viral replication (such as Polo-like kinases)[6][2].
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