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Rotavirus structural and non-structural proteins constitute the functional and architectural components of the rotavirus, a leading cause of severe diarrhea in children worldwide [1]. The structural proteins (VP1, VP2, VP3, VP4, VP6, and VP7) form the triple-layered viral particle and facilitate host cell attachment, entry, and the transcription of the viral genome [2]. Specifically, VP4 and VP7 are the primary targets for neutralizing antibodies induced by current vaccines like Rotarix and RotaTeq [3]. The non-structural proteins (NSP1-NSP6) are produced during the viral life cycle to coordinate replication, assembly, and immune evasion [1]. Notably, NSP4 acts as a viral enterotoxin that disrupts calcium signaling, leading to secretory diarrhea, while NSP1 antagonizes the host interferon response [4]. Therapeutic strategies focus on preventing infection through vaccination or managing symptoms, with ongoing research into small-molecule inhibitors targeting the viral polymerase (VP1) or the enterotoxin (NSP4) [2, 3].
Vaccines induce neutralizing antibodies against VP4 and VP7 to prevent viral entry; antiviral agents like nitazoxanide may interfere with viral replication and maturation.
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