# Rhinovirus Infects B and CD4 T Lymphocytes in Hypertrophic Tonsils in Children

## TL;DR

This study shows that rhinovirus infects immune cells in children's enlarged tonsils, which may explain prolonged viral shedding and impact the immune system.

## Contribution

The study identifies B and CD4 T lymphocytes as new host cells for rhinovirus in hypertrophic tonsils.

## Key findings

- Rhinovirus infects tonsillar epithelial surfaces, parenchyma, and immune cells like B and CD4 T lymphocytes.
- Infectious rhinovirus was recovered from adenoids and respiratory secretions of children with tonsillar hypertrophy.
- In vitro experiments showed viral replication and distinct cytokine profiles in infected tonsillar mononuclear cells.

## Abstract

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.