Purpose of review: In recent years, many investigators have focused on potential associations between infections and vascular inflammation. We review the principal pathogenic mechanisms that have been implicated for possible roles in the vascular inflammation initiated by infectious agents. We also summarize the most important literature related to this topic.
Recent findings: A novel theory known as autoantigen complementarity suggests that an infectious agent could trigger antineutrophil cytoplasmic antibody-associated vasculitis. Several recent studies investigating the presence of parvovirus B19 and herpesviruses in temporal arteries with giant cell arteritis have yielded contradictory results. A recent study has identified higher frequency of a novel human virus, the 'New Haven coronavirus', in respiratory secretions of children with Kawasaki disease. Many case reports have suggested potential relationships between human pathogens and vasculitis.
Summary: There remains considerable interest in the possibilities of primary vasculitic syndromes caused in some fashion by infection. With the exception of a few well sustained associations - for example hepatitis B or C with known vasculitic syndromes - most of the purported links between microbial agents and primary vasculitides remain speculative.