Parvovirus and autoimmune diseases

Abstract

For decades, the role of viruses in the initiation and exacerbation of autoimmune disorders have been widely documented. Recently, a growing number of studies have been questioning the relationship between human parvovirus B19 infection and autoimmune disorders. The reason behind a possible association was based on three key findings: (1) the similarities of the clinical manifestations of parvovirus B19 infection with certain autoimmune diseases such as systemic lupus erythematosus (SLE); (2) the production of parvovirus B19 viral protein-induced antibody against self-antigens such as cardiolipin, single-stranded DNA, keratin, and collagen type II; (3) high prevalence of parvovirus B19 DNA as well as positive serological tests of parvovirus B19 in patients with autoimmune diseases. However, the virus-host interactions leading to autoimmune response after parvovirus B19 infection remain uncertain. Nevertheless, three mechanisms were proposed as an explanation for evoking an autoimmune response following infection: molecular mimicry, self-antigen presenting to T cells caused by parvovirus B19-induced erythroblast apoptosis, and the phospholipase activity of the unique region of parvovirus B19 VP1 protein. In fact, the importance of revealing the role of parvovirus B19 infection in autoimmune response particularly in the light of new therapeutic perspectives cannot be overemphasized. Therefore, in this chapter we review the mechanisms related to autoimmune disorders secondary to parvovirus B19 infection. Diseases such as SLE, autoimmune-mediated heart diseases like myocarditis and dilated cardiomyopathy, as well as autoimmune hemolytic anemia are all presented and discussed.