Objective: HDL function rather than absolute level may be a more accurate indicator for cardiovascular disease (CVD) but it is unclear what drives HDL dysfunction in HIV-1 infection. The objective of this study is to identify factors that may contribute to HDL dysfunction in chronic HIV-1 infection.
Design: Retrospective study of HIV-1 infected males with low overall CVD risk and healthy males with no known CVD risk matched by race to the HIV-1 infected participants.
Methods: We related parameters previously reported to be associated with HDL function to two different measures of HDL function: reduced antioxidant function (oxidized HDL, HDLox) and HDL-apoA-I exchange (HAE). Multivariable-adjusted linear regression analyses were employed adjusting for false discovery rate (FDR), age, race, body mass index (BMI), CD4 count, viremia, CVD risk, smoking, lipids, apoA-I, albumin.
Results: In multivariate analysis among HIV-1 infected males (n=166) (median age 45 years, median CD4 T cell count 505 copies/ml, 30.1% were viremic), higher BMI, lower apoA-I and lower albumin were among the most notable correlates of higher HDLox and lower HAE (impaired HDL function)(p<0.05). In HIV-1 uninfected participants lower albumin and higher BMI were associated with lower HAE and higher HDLox, respectively (p≤0.05). HDLox was inversely related to HAE in HIV-1 infected (but not uninfected) individuals (p<0.001).
Conclusion: Increased HDLox is associated with reduced HDL remodeling in chronic HIV-1 infection. Higher BMI, lower apoA-I and lower albumin were identified as factors associated with abnormal HDL function in chronic HIV-1 infection using two independent methods.