The human immunodeficiency virus (HIV), the human T cell lymphotropic virus (HTLV-1), the human foamy retrovirus and the simian immunodeficiency viruses have been associated with the development of an
inflammatory myopathy in humans and primates. The
myopathy caused by HIV and HTLV-1 is not due to direct
infection of the muscle by these viruses, but rather due to an immunopathologic process triggered by the viruses, mediated by autoaggressive CD8+ cells in the context of MHC-
class I antigen expression. This has been based on a series of studies utilizing immunocytochemistry, in situ hybridization, polymerase chain reaction, and co-cultivation of human myotubes with the viruses or with HIV-1 and HTLV-1-infected homologous lymphoid cells. Because the clinical, histological and immunological picture of patients with retroviral-associated
inflammatory myopathies is identical to that of patients with retroviral-negative
inflammatory myopathy, there is a reasonable possibility that retroviruses may be candidate viruses in triggering
inflammatory myopathies. In recent years, the antiretroviral
drug AZT (
Zidovudine), commonly used for the treatment of
AIDS, has been shown to cause a distinct
mitochondrial myopathy characterized by depletion of the muscle
mitochondrial DNA due to AZT's ability to inhibit the gamma-
DNA polymerase of the mitochondrial matrix. Distinction of the AZT-
myopathy is clinically important because it responds to discontinuation of AZT and to administration of another
antiretroviral agent such as ddI or ddC.