Smoking may affect cardiovascular disease risk more strongly in human immunodeficiency virus (HIV)-infected individuals than HIV-uninfected individuals. We hypothesized that an interaction at the level of the immune system may contribute to this increased risk. We assessed soluble markers of inflammation (high-sensitivity C-reactive protein [hsCRP]), immune activation (soluble [s]CD14 and sCD163), and coagulation (D-dimer) in HIV-infected and uninfected never, former, and current smokers. Smoking was independently associated with higher hsCRP levels and lower sCD163 levels and was borderline significantly associated with higher sCD14 and D-dimer levels. We found no evidence of a differential effect of smoking in HIV-infected individuals as compared to uninfected individuals.
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