Key result
Immunohistochemistry and in situ hybridization fail to detect HTLV-I signals in polymyositis muscle biopsies.
Why the study?
Are HTLV-I products detectable by in situ hybridization in the biopsied muscles of viral carriers with polymyositis?
Observational (n=6)
No
Are HTLV-I products detectable by in situ hybridization in the biopsied muscles of viral carriers with polymyositis?
HTLV-I does not appear to directly infect muscle fibers in patients with polymyositis who are infected with HTLV-I alone, suggesting that HIV co-infection may be necessary for direct viral expression in muscle.
No HTLV-I detection in monoinfected polymyositis muscle warrants caution against direct viral attribution; leaves open HIV co-infection as possible requirement for expression.
Direct infection of muscle fibers by human T-lymphotropic virus type I (HTLV-I) has recently been reported in a patient with polymyositis infected with both HTLV-I and human immunodeficiency virus (HIV). Coinfections of these viruses are frequently found in the United States. In Kagoshima, Japan, patients with polymyositis have a significantly increased incidence of seropositivity to HTLV-I alone, when compared with the general population of Kagoshima. In this study, we examined muscle tissue from 6 HTLV-I-positive patients with polymyositis from Kagoshima. To detect HTLV-I products, sensitive immunohistochemistry and in situ hybridization analysis were performed. These were compared with muscle fibers from a well-characterized transgenic mouse model which expressed HTLV-I tax. No specific signals were detected in the biopsied muscles of patients with polymyositis infected with HTLV-I alone. HIV co-infection may, therefore, augment HTLV-I expression through either immunosuppression or direct viral interactions.
No takes yet. Share an insight, caveat, or question.
Higuchi et al. (1992) conducted an observational in Polymyositis with HTLV-I infection (n=6). HTLV-I infection alone vs. Transgenic mouse model expressing HTLV-I tax was evaluated on Detection of HTLV-I products by immunohistochemistry and in situ hybridization. Immunohistochemistry and in situ hybridization failed to detect specific HTLV-I signals in the biopsied muscles of 6 patients with polymyositis infected with HTLV-I alone.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: