the influence in virus infections in COPD

 Chronic obstructive pulmonary disease (COPD) is extensively influenced by viral infections. Human adenovirus, non-respiratory viruses, and respiratory syncytial virus are especially important for the pathogenesis and course of COPD.Acute exacerbations of chronic obstructive pulmonary disease are thought to be caused by complex interactions between the host's individual microbiome, bacteria, viruses, and environmental influences.Respiratory viral infections lead to desquamation, microvascular dilatation, edema, and inflammatory cell infiltrate, which predispose the lower airways to bacterial infections and increase the duration of hospital stay.Viral infections are the most important causes and very common in COPD exacerbations. Combined bacterial and viral infection can be identified in 25% of exacerbations, and these dual infections are often more severe, although this increased severity is not confirmed by all studies. In the lungs of humans with COPD, the innate immune system is activated by viral infections, leading to increased numbers of invariant natural killer T-cells and alternatively activated IL-13-producing macrophages, as well as increased symptomatology and mortality.Cigarette smoke enhances parenchymal and airway inflammation, as well as apoptosis, emphysema, and airway fibrosis, which are induced by the viral pathogen-associated molecular pattern (PAMP) poly(I:C).eespiratory viruses are important triggers of acute exacerbations and 'key players' in COPD pathogenesis. Childhood respiratory infections are an independent risk factor for the subsequent development of COPD, and the presence of a virus in upper airway secretions is strongly associated with the development of COPD exacerbations.Some viruses, such as RSV, stimulate the helper T-lymphocyte type 2 (Th2)-pattern of immune responses, which is associated with allergic inflammation.Infections are frequently associated with COPD exacerbations, and patients with infectious exacerbations suffer from prolonged hospitalizations and greater impairment of several lung function parameters than those with non-infectious exacerbations. Sputum inflammatory markers are increased at the time of acute COPD exacerbation and then decline 1 month later.