HIV infection leads to a gradual but persistent loss of host immunity that results in a syndrome of immune dysregulation, dysfunction, and deficiency(1). Initial infection with HIV leads to large depletion of CD4+ effector-memory lymphocytes from mucosal-associated lymphoid tissue. There is generalised immune activation leading to progressive decline in naïve and memory T cell pool that results in systemic CD4+ lymphocyte depletion during the chronic phase of the infection. HIV infection is also associated with B cell dysfunction, hypergammaglobulinemia, and defective specific antibody responses (2). The combination of immune dysfunction, dysregulation, and depletion of CD4 + lymphocytes result in increased risk of infections in untreated patients. Among people living with HIV (PLHIV) treated with anti-retroviral therapy, chronic inflammation and immune activation decrease; however, immune activation can persist in patients who started ART at lower CD4+ cell counts or in those whose treatment is interrupted (3, 4).  

 HIV infection causes alteration in several lines of host defenses in the lung and respiratory tract that contribute to an increased risk of lung complications (1). HIV alters mucociliary function and soluble defense molecules in respiratory secretions.  Within the lung parenchyma, innate and adaptive immune responses to pathogens may be impaired. For example, alveolar macrophages from HIV-infected individuals have been shown to be deficient in pathogen recognition. HIV also results in chronic stimulation and activation of inflammatory cells within the alveolar space(1, 5) The bronchoalveolar lavage (BAL) fluid from HIV infected individuals early in infection has demonstrated higher numbers of polyfunctional CD4+ T cells, in contrast to the depletion of CD4+ T cells seen in gut mucosa (6). In early-to mid-stage disease, HIV infected individuals have increased numbers of HIV-specific CD8+ T lymphocytes which secrete high amounts of IFN-y within the alveolar space(7). Within the lung, HIV can infect the alveolar macrophages, T cells and fibroblasts. Evidence suggests that T cells may be a long-lived reservoir of infection within the lung (8). 

HIV is associated with a broad spectrum of lung diseases and many infectious and non-infectious complications have been described (9-11). These include diseases that are AIDS-defining or HIV-associated such as Pneumocystis pneumonia and pulmonary tuberculosis, disorders that are not classified as AIDS-defining but are more common in patients with HIV infection (e.g., lung cancer, pulmonary arterial hypertension, and chronic obstructive pulmonary disease), and conditions whose association with HIV is inconclusive or coincidental (e.g., sarcoidosis). In addition, lung complications can result from immune reconstitution inflammatory syndrome (also called immune reconstitution syndrome), which may occur after initiation of ART(12).  

As people living with HIV (PLHIV) are living longer, non-infectious complications and co-morbid conditions have increased in frequency in the last couple of decades(13). The increased risk of non-infectious respiratory diseases in PLHIV was first demonstrated in a study from the United States by Crothers et al. Data from 33,420 HIV-infected and 66,840 age, sex, race, ethnicity, and size-matched HIV-uninfected veterans were analysed to determine the association of HIV with pulmonary diseases. The study demonstrated that the HIV infected cohort had a greater risk of chronic obstructive pulmonary disease, lung cancer, pulmonary hypertension and pulmonary fibrosis compared to HIV-uninfected cohort (14). Subsequent studies have confirmed the findings of the study by Crothers et al (15, 16). The rise in incidence of non- infectious lung complications in PLHIV has been shown in a nation-wide French study that examined the rates of hospitalisations due to non-infectious lung diseases between 2007 and 2013. The study demonstrated that there was a significant increase in incidence from 45.6% to 54.7% in people hospitalised with non-infectious lung diseases between 2007 and 2013 (17).