Anti-apolipoprotein A-1 autoantibodies are associated with immunodeficiency and systemic inflammation in HIV patients. Journal of Infection. Â Journal of Infection
Satta et al. aimed to determine the existence of autoantibodies against apolipoproteinA-1 (anti-apoA-1 IgG) in HIV patients and explore their association with biological features of HIV infection and different inflammatory biomarkers. So far, anti-apoA-1 IgG positivity has been shown to vary between 0 and 5% in healthy blood donors, 20% in the general population, and reaching 30% in high CV risk populations.
Anti-apoA-1 IgG plasma levels were assessed by ELISA in 237 HIV positive patients from the Swiss HIV Cohort Study with no current lipid-lowering therapy.
Fifty-eight percent of patients were found positive for anti-apoA-1 IgG and were associated with lower CD4+ counts, but higher viremia and systemic inflammation. Logistic regression analyses indicated that high anti-apoA-1 IgG levels were associated with a 16-fold increased risk of displaying low CD4+ levels, independent of HIV RNA levels and treatment (adjusted Odds ratio [OR]:16.1, 95% Confidence Interval [95%CI]:1.80–143.6; p = 0.01), and a 6-fold increased risk of having a detectable viremia, independent of antiretroviral treatment (OR:5.47; 95% CI:1.63–18.36; p = 0.006). In vitro, anti-apoA-1 IgG induced dose and time-dependent CD4+ apoptosis that was increased by exposure to HIV RNA.
In conclusion, this hypothesis generating pilot study indicates that anti-apoA-1 IgG levels are increased and associated with a pro-inflammatory cytokine profile, lower thrombocytes, CD4+ counts, and higher viremia. Furthermore, experimental evidence showed that stimulation with anti-apoA-1 IgG can negatively affect CD4+ lymphocyte survival trough novel and yet undefined pathways, an effect that was magnified by the concomitant presence of HIV RNA in vitro. Taken together, these results indicate that anti-apoA-1 IgG may represent a relevant prognostic biomarker in HIV patients. This working hypothesis needs to be challenged in large multicentre longitudinal trials before extrapolating the possible clinical implications of the present findings.