Thus, one could speculate that PLWH may experience different phenotypes of emphysema than uninfected controls, as a consequence of pathological mechanisms mediated by up-regulation of inflammatory markers such as TNFα and IL-1β which could explain the higher prevalence of respiratory symptoms in PLWH compared to uninfected controls, previously found in our and other cohorts (8, 34). Here, IL1B is linked to pulmonary emphysema.