Reactive arthritis ReA is still an incompletely understood rheumatic disorder whose immunopathogeny involves several mechanisms. There is an association with Class-I histocompatibility antigens HLA-B27 and history of previous gastrointestinal or genitourinary infections. The molecular mimicry between bacterial and self antigens suggests the possibility of cross reactivity as a disease mechanism. The infection pandemics by the human immunodeficiency virus HIV changed the profile of the occurrence of a number of rheumatic diseases including ReA which appears to be more frequent more severe and refractory to the usual treatment for retrovirus-infected patients. The intensity of articular and extra-articular manifestations of ReA often makes the use of immunosuppressant drugs in these patients necessary. Due to the immunosuppression resulting from the retrovirosis itself the treatment becomes a dilemma for rheumatologists. HIV seems to play a role in the main ReA immunopathogenesis mechanisms either acting as direct arthritogenic agent or causing an immune dysfunction in the CD4 T lymphocytes T CD8 relationship leading to the deregulation in the production of cytokines or in advanced immunosuppression stages predisposing to infection by other arthritogenic pathogens. The use of highly active anti-retroviral therapy HAART has changed the profile of rheumatic events and the immunopathogeny of the HIV ReA association. The understanding of the basic ReA immunopathogenic mechanisms in HIV-infected patients is vital in the attempt of elucidating many still existing questions.