Purpose of review: To provide an update about the interactions between infections and autoimmune diseases (AIDs), from the molecular perspective to the clinical spectrum and the differentiation between infection and disease activity.
Recent findings: Any kind of infection may modify the innate and adaptive immune response through the following mechanisms: molecular mimicry, superantigens, epitope spreading and B-cell activation. The consequence is the overproduction of antibodies shared with those found in AIDs. Viral infections, especially HIV and hepatitis C virus, can stimulate the production of antiphospholipid antibodies and confer an increased risk to develop antiphospholipid syndrome.
Summary: The identification of risk factors to develop infections in patients with AIDs is remarkable to prevent them. These factors are the use of steroids and immunosuppressants, the involvement of a major organ (lungs, brain and kidney) and severe activity. Biomarkers to differentiate infection from disease activity are scarce, but the combination of procalcitonine and C-reactive protein seems to have higher specificity and sensibility to identify infections in patients with AIDs. Finally, the clinical judgment is the hallmark to differentiate between infections and disease activity.