Comparison of immune response to human rhinovirus C and respiratory syncytial virus in highly differentiated human airway epithelial cells

Virology Journal

Yu Jin¹  Xin-hui Yuan¹  Jing Yang²  Li-li Pang³ 

[1] Medical School of Nanjing University;Nanjing Children’s Hospital Affiliated to Nanjing Medical University;National Institute for Viral Disease Control and Prevention, Chinese Center for Disease Control and Prevention;

关键词: Human rhinovirus C;    Air–liquid interface;    Human bronchial epithelial cell;    Respiratory syncytial virus;    Immune response;    Cytokines;   

DOI  :  10.1186/s12985-022-01805-2

来源: DOAJ

【 摘 要 】

Abstract Background Human rhinovirus C (HRV-C) accounts for a large proportion of HRV-related illnesses, but the immune response to HRV-C infection has not been elucidated. Our objective was to assess the effect of HRV-C on cytokine secretion in human bronchial epithelial (HBE) cells grown at air–liquid interface (ALI) and compare it with that of respiratory syncytial virus (RSV). Methods HBE cells were differentiated at ALI culture and the full-length cDNA clones of HRV-C651 and HRV-C15, clinical isolates of HRV-C79 and HRV-C101, and two RSV isolates were inoculated in the HBE cells. The effect of HRV-C on cytokine secretion was assessed and compared with that of RSV. Results HRV-Cs infect and propagate in fully differentiated HBE cells and significantly increase the secretion of IFN-λ1, CCL5, IP10, IL-6, IL-8, and MCP-1. The virus loads positively correlated with the levels of the cytokines. HRV-C induced lower secretion of CCL5 (P = 0.048), IL-6 (P = 0.016), MCP-1 (P = 0.008), and IL-8 (P = 0.032), and similar secretion of IP10 (P = 0.214) and IFN-λ1 (P = 0.214) when compared with RSV. Conclusion HBE ALI culture system supported HRV-C infection and propagation and HRV-C induced relatively weaker cytokine expression than RSV.

【 授权许可】

Unknown