Angel Rico, MiguelTrento, AlfonsinaMelero, Jose AntonioRamos, ManuelJohnstone, CarolinaVal, Margarita delLopez, Daniel2020-07-062020-07-062009Immunol Cell Biol . May-Jun 2009;87(4):344-50.0818-9641http://hdl.handle.net/20.500.12105/10654Human 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.engAMhttp://creativecommons.org/licenses/by-nc-sa/4.0/AnimalsB-LymphocytesBiomarkersCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesGlycosaminoglycansHistocompatibility Antigens Class IHistocompatibility Antigens Class IILymphocyte ActivationMiceMice, Inbred C57BLRespiratory Syncytial Virus InfectionsRespiratory Syncytial Virus, HumanAtribución-NoComercial-CompartirIgual 4.0 Internacional19153593874344-5010.1038/icb.2008.109Immunology and cell biologyopen access