State of the Art: What We Know About Infectious Agents and Myositis

Lu Gan; Frederick W. Miller


Curr Opin Rheumatol. 2011;23(6):585-594. 

In This Article

Viruses and Idiopathic Inflammatory Myopathy

The association between viral infections and onset of IIM has a longer history and the evidence appears stronger than that for other pathogens. Epstein–Barr virus (EBV) is a human herpesvirus that resides in a latent form in memory B cells in the majority of the world population and has been reported to be related to the development of a number of autoimmune disorders.[48] A case– control study[16••] showed evidence for higher frequencies of anti-Epstein–Barr nuclear antigen 1 (EBNA1) antibodies at the onset of dermatomyositis/polymyositis and the EBV genome was detected in a higher frequency of patients than in the matched healthy controls. In this study, the concurrence of malignancies such as nasopharyngeal carcinoma (NPC) further increased the risk of development of IIM. In addition, a case report from Japan described the development of polymyositis after EBV infection.[17] Interestingly, a case report of EBV infection was associated with the development of concurrent JDM and type 1 diabetes.[18] Another study,[19] however, did not replicate these findings in JDM patients.

Hepatitis viruses and their vaccines have been proposed to be involved in the development of IIM. Case reports suggest a possible association between exposure to hepatitis B virus and the onset of IIM,[20] as well as a possible association with hepatitis C virus infection.[21–23] In addition to the direct viral infection detected in IIM patients, indirect evidence of the role of viral vaccine-related IIM was also discussed in some previous case reports.[49,50]

Another category of viruses, retroviruses, which include HIV and human T-lymphotropic virus 1 (HTLV-1), has been related to development of IIM in case reports.[24,27] Thirteen patients were reported to develop polymyositis after HIV infection, with an average time of 4.3 years from viral infection to disease onset[26] and four patients who developed IBM after exposure to HIV were also studied.[25] A study of 11 Japanese patients with IBM[28] and a report of three British patients with polymyositis[29] both detected anti-HTLV-1 antibodies in sera of all the patients. Additionally, two separate studies of polymyositis patients from Jamaica reported 63%[30] and 87.5%[31] as having serological evidence of prior HTLV-1 infection, respectively. Detection of the viral genome in muscle biopsies further supported the association between HTLV-1 and polymyositis.[31]

Although there is evidence that parvovirus B19 infection may be related to certain autoimmune disorders such as rheumatoid arthritis,[51] less convincing data exist for the role of parvovirus B19 in the development of IIM. Case reports, including that of an adult with dermatomyositis[32] and two children with JDM,[33,34] have suggested an association. Nonetheless, a carefully conducted case–control study[35] did not find an increased prevalence of antiparvovirus B19 IgG in the plasma of patients with JDM and a low level of viral DNA was detected in the patients' muscle tissues. Another negative result was found in a case series of seven patients with polymyositis/dermatomyositis.[36]

Enteroviruses, which include coxsackieviruses (group A and B) and enteric cytopathogenic human orphan (ECHO) viruses, are potential candidates for inducing IIM based on previous findings of enteroviral RNA in muscle biopsies.[37] However, some studies failed to detect enteroviral RNAs in muscle biopsy samples of JDM patients[38] or coxsackievirus B (CVB) genomes in IIM patients.[39] Similarly, in a case–control study[40] of new-onset JDM, elevated antibody titers for enteroviruses were detected at the same rates in both patients and healthy controls, suggesting that enteroviral infection might simply be a common environmental exposure rather than a trigger for JDM.

Recently, a case–control study[41] in Hungary detected the infection of a novel virus, Torque teno virus (TTV), in both IIM patients and healthy controls. There was no obvious association between the viral infection and the development of IIM, but the higher frequency of TTV infection in severe cases than in mild ones suggested that this viral infection may lead to a more severe IIM.

Influenza virus was previously reported to be associated with polymyositis[52] and dermatomyositis.[53] Cases of dermatomyositis have also been reported following influenza vaccines, raising the possibility that immune responses to antigens shared by the virus and vaccine could be implicated in the development of myositis.[54,55]