Human respiratory syncytial virus (HRSV) is the most common cause of severe respiratory infections in infants and young children, often leading to hospitalization. Although human airway epithelial cells are the main target of HRSV, it has been reported that this virus can also infect professional antigen-presenting cells such as macrophages and dendritic cells, promoting upregulation of maturation markers. Here, we report that mouse spleen B220(+) B lymphocytes were susceptible to HRSV infection in vitro, probably involving a glycosaminoglycan-dependent mechanism. In contrast, neither CD4(+) nor CD8(+) T lymphocytes were infected. In B lymphocytes, HRSV infection upregulated major histocompatibility complex (MHC) class II but not MHC class I molecules and induced the expression of the activation marker CD86.
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Rico et al. (2009) studied this question.
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