How could infectious agents hide in synovial cells? Possible mechanisms of persistent viral infection in a model for the etiopathogenesis of chronic arthritis.

Abstract

It has been hypothesized that a persistent intra-articular viral infection might play an important part in the pathogenesis of chronic arthritis. However, it remains unclear how such an infection could survive in synovial cells that express large amounts of HLA-DR and intercellular adhesion molecule-1 (ICAM-1) by which they communicate with immunocompetent cells. In an in vitro model of persistent mumps virus infection of synovial cells, results suggested that, in contrast to mock-infected cells, cells containing viral antigen did not express HLA-DR in response to interferon-gamma and that they did not up-regulate ICAM-1 expression under these conditions. Previously it has been shown that infected synovial cells do not express viral surface antigens. By these mechanisms, infected cells, interspersed among a large majority of uninfected cells, might evade recognition and eradication by the immune system. Lack of neoantigen expression on infected cells might be an important viral strategy to maintain a persistent infection and to initiate and perpetuate joint inflammation.