Cellular senescence has been implicated in COPD pathogenesis. Severe COPD is associated with exacerbations, hospitalisations and increased mortality. Airway inflammation and emphysema present many overlapping hallmark characteristics of senescence. However, features of bronchial epithelial senescence in severe COPD inflammation and in virus-induced exacerbations are not well understood. To address this, we characterised well-differentiated primary bronchial epithelial cells (WD-PBECs) derived from severe COPD patients undergoing lung transplantation and compared them to age-matched healthy controls using the air-liquid interface (ALI) culture model. Single-cell RNA-sequencing was carried out to identify the transcriptomes of the two cultures before and after rhinovirus infection. Expression of senescence markers and senescence-associated secretory phenotype (SASP) were analysed. The senescence markers p16-INK4A, p21Waf1/Cip1 and p53 were increased in COPD cultures compared with healthy controls. HRV infection further exacerbates SASP in COPD. A series of interferon-associated genes which upregulated in healthy subjects in response to rhinovirus infection were completely lost in infected COPD cultures. There were dramatically reduced levels of IL29 (IFNλ) in HRV infected COPD compared with healthy subjects. Our data demonstrate that the epithelium in severe COPD displays a senescent phenotype in terms of increased expression of senescent markers and SASP associated inflammatory response. After HRV infection there was further heightened COPD inflammation by elevated secretion of SASP and, importantly, there was impaired interferon anti-viral responses in COPD.