Background:  Increasing evidence suggests an association between HIV and obstructive lung disease (OLD). In prior cross-sectional analysis, we showed that higher serum HIV viral load was associated with increased odds for OLD. Longitudinal data characterizing lung function decline among HIV⁺ and at-risk persons have not been reported. We hypothesized that HIV disease markers would be associated with more rapid lung function decline.

Methods:  Semi-annual clinical, laboratory, and spirometric data were collected in the AIDS Linked to the IntraVenous Experience (ALIVE) study, an observational cohort of HIV⁺ and HIV^– injection drug users in Baltimore, Maryland. Repeated measure random-effects models estimated the independent effects of HIV infection, RNA levels, and CD4 cell count on annual decline in forced expiratory volume in one second (FEV1) after adjusting for baseline demographics and time-varying smoking status.

Results:  Among 1064 participants, we performed 4555 spirometry measurements during a median of 2.75 years (range 0.5 to 3.9) of observation. At baseline the cohort was 49 ± 7 years old, 65% male, 91% African American, 30% HIV⁺ and >94% were current or former smokers. The prevalence of OLD was 16% and did not differ by HIV status (p = 0.74). After adjustment for age, sex, race, body mass index, and smoking pattern, HIV-infection was associated with a 174 mL lower absolute FEV1 (p <0.01). The annual rate of FEV1 decline among HIV negative persons (–24.2 mL/year) did not differ significantly between HIV⁺ persons with undetectable HIV RNA (–35.7 mL/year) or RNA of 400 to 75,000 copies/mL (–28.3 mL/year). However, HIV⁺ persons with HIV RNA >75,000 copies/mL had significantly greater annual FEV1 decline (–107 mL/year; p = 0.003); these associations persisted after adjusting for ART use. Similarly, persons with CD4 cell counts from 100 to 200 and <100 cells/mm³ were associated with more rapid FEV1 decline (–61.4 and –85.6mL/year; p = 0.025 and 0.017, respectively).

Conclusions:  Markers of advanced and uncontrolled HIV disease were associated with more rapid decline in lung function. The decline seen with high viral load is greater than the 50 to 70 mL/year decline seen in smokers. These findings expand the current state of knowledge regarding the association between HIV infection and chronic lung disease and suggest that optimal ART with HIV virological suppression may diminish the accelerated decline in lung function.