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Demonstrates rhinovirus infection of T and B lymphocytes in hypertrophic tonsils, suggesting prolonged virus shedding.
Prolonged detection of rhinovirus (RV) in secretions after a typical cold and asymptomatic shedding are frequently reported. Although RV has been detected in human hypertrophic tonsils, its replicative status and host cell range remain unclear. In this study, we analyzed RV replication, infected cell types, and recovery of infectious virus in adenoids, palatine tonsils, and respiratory secretions from 293 children with tonsillar hypertrophy undergoing tonsillectomy. Samples were screened by real‐time RT‐PCR, and RV‐positive samples were analyzed using immunohistochemistry (IHC), chromogenic in situ hybridization (CISH), flow cytometry, and RV isolation in cell culture. RV genotypes from species A, B, and C were identified in adenotonsillar samples. RV antigenome and structural proteins were detected in tonsillar epithelial surfaces, parenchyma, and in CD4 + T and B lymphocytes. Infectious RV was recovered from adenoids and respiratory secretions. In vitro infection of tonsillar mononuclear cells with RV‐16 and RV‐1A resulted in viral progeny production and secretion of distinct cytokine profiles. These findings demonstrate that RV infects tonsillar T and B lymphocytes, suggesting that tonsils can serve as sites of prolonged infection and sources of RV shedding. RV infection of immune cells may have potential impact on the local immune microenvironment.
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Martins et al. (2026) studied this question.
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