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Intracellular invasion is a complex biological process through which pathogenic organisms, including viruses, bacteria, and parasites, gain entry into host cells to facilitate their survival and replication (10). This multi-step phenomenon typically begins with the specific attachment of pathogen surface ligands to host cell receptors, followed by the activation of cellular signaling pathways that trigger internalization via mechanisms like receptor-mediated endocytosis, macropinocytosis, or direct membrane fusion (3, 7). Once inside, pathogens may reside within membrane-bound vacuoles or escape into the cytoplasm to evade host immune defenses such as antibodies and complement proteins (1, 6). Because it encompasses a wide array of distinct molecular interactions involving various host and pathogen factors, intracellular invasion is characterized as a biological phenomenon rather than a single molecular target. Therapeutic strategies targeting this process, often termed entry inhibitors or host-directed therapies, aim to prevent the initiation of the infection cycle by blocking these early interactions or enhancing the host's ability to clear invaded pathogens (2, 9).
Inhibition of pathogen-host receptor binding, blocking of membrane fusion, disruption of endocytic pathways, or induction of host-directed autophagy to clear internalized pathogens.
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