Infection by the human immunodeficiency virus (HIV) is characterized by chronic immune activation, progressive depletion of CD4+ T lymphocytes, and gradual decline in immune function. Several autoimmune phenomena have been described in people living with HIV/AIDS (PLHIV), including circulating autoantibodies such as anticardiolipin IgG (aCL IgG), associated with antiphospholipid syndrome and venous thrombosis; anti-dsDNA, associated with systemic lupus erythematosus; and antineutrophil cytoplasmic antibodies (p-ANCA/c-ANCA), associated with systemic vasculitides, suggesting a complex interplay among viral infection, immune dysregulation, and autoimmunity.

To evaluate the frequency of aCL IgG, anti-dsDNA, and ANCA and the effects of antiretroviral therapy (ART) on immune response in a cohort of PLHIV after 1 and 2 years of therapy.

In this longitudinal study, approved by the ethics committee (CAAE 66529116.4.0000.5634), a cohort of 50 PLHIV in Belém/PA was assessed before and after 1 and 2 years of ART. CD4+ and CD8+ T-cell counts, viral load, and presence of aCL IgG, anti-DNA, and pANCA-cANCA were analyzed.

After ART, CD4+ T-cell counts increased progressively, along with the number of individuals with undetectable viral load. aCL IgG was more reactive in ART-naïve individuals and decreased significantly after 2 years of therapy (p = 0.0003). Anti-dsDNA and p-ANCA/c-ANCA showed no significant differences. By CD4+ level and viral load, the group with < 200 cells/µL had the highest frequencies of anti-dsDNA, p-ANCA/c-ANCA, and aCL IgG compared with 200 to < 350 and ≥ 350 cells/µL; only aCL IgG reached statistical significance (p = 0.0083). Higher viral loads were associated with higher aCL IgG frequencies (p < 0.0001). Differences in anti-dsDNA and p-ANCA/c-ANCA were not significant.

Our study underscores the importance of monitoring autoantibody profiles in PLHIV, particularly in the context of ART-mediated immune recovery. The association between aCL IgG and severe immunosuppression supports the hypothesis that sustained viral replication induces chronic inflammation and B-cell activation, favoring IgG autoantibody production. This reinforces the link between dysregulated immune activation and autoimmunity in HIV, and the role of ART in reducing viral load and systemic inflammation, thereby decreasing the frequency of these autoantibodies.