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Human rhinoviruses (RVs) are the leading cause of the common cold and among the most prevalent infectious agents affecting humans worldwide. Although RV infections of the upper respiratory tract are generally mild and self-limiting, accumulating evidence demonstrates that RVs can contribute to substantial morbidity beyond uncomplicated cold symptoms. RV infections are increasingly recognized as important triggers of asthma and chronic obstructive pulmonary disease exacerbations, severe lower respiratory tract infections in vulnerable populations, and secondary bacterial infections. Despite their clinical relevance, the molecular and immunological mechanisms underlying RV-associated complications remain incompletely understood. Like many successful pathogens, RVs have evolved multiple strategies to modulate and evade host immune responses. Advances in virology, immunology, and omics-based technologies have substantially improved our understanding of RV–host interactions, including viral interference with innate immune signaling pathways, epithelial barrier function, interferon responses, adaptive immunity and cell metabolism. In this review, we summarize current knowledge regarding the immune evasion and immunomodulatory mechanisms employed by RVs and discuss how these processes may contribute to altered immune competence and disease pathogenesis in humans.
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Johannes Stöckl (2026) studied this question.
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