OBJECTIVE: To determine the presence of antibodies that bind vesicular stomatitis virus (VSV) proteins in systemic lupus erythematosus (SLE) patient sera, as well as to examine any relationship between antibodies binding the viral nucleocapsid (N) protein and anti-Ro autoantibodies. METHODS: Eighty SLE patient sera, 80 normal control sera, 47 rheumatic disease patient control sera, and 9 sera from Panamanian subjects (6 of whom were infected with VSV) were evaluated by immunoblot of purified VSV proteins. RESULTS: Findings on immunoblots of the Panamanian subjects' sera were consistent with histories of endemic exposure to VSV, as determined by virus neutralization assays. Significantly different binding to viral proteins was seen in the group of 80 SLE patients compared with the normal control group and with the rheumatic disease control group, by a variety of measures. For example, most of the reactivity in the SLE patient sera included binding to the internal viral matrix (M) and N proteins, while the reactivity in the normal control sera was mostly against the surface viral glycoprotein (G) protein alone or the N protein alone. Within this SLE patient cohort, associations were found between binding to N protein and anti-Ro precipitins and between binding to M protein and anti-nuclear RNP autoantibody precipitins. CONCLUSION: The data are consistent with the original specific hypotheses of a relationship between 60-kd Ro autoantigenicity and VSV, as well as with the suggestion that a rhabdovirus may be important in SLE. They do not, however, make possible any conclusions concerning the role of rhabdoviruses in the development of SLE or of anti-Ro autoimmunity.
OBJECTIVE: To determine the presence of antibodies that bind vesicular stomatitis virus (VSV) proteins in systemic lupus erythematosus (SLE) patient sera, as well as to examine any relationship between antibodies binding the viral nucleocapsid (N) protein and anti-Ro autoantibodies. METHODS: Eighty SLEpatient sera, 80 normal control sera, 47 rheumatic diseasepatient control sera, and 9 sera from Panamanian subjects (6 of whom were infected with VSV) were evaluated by immunoblot of purified VSV proteins. RESULTS: Findings on immunoblots of the Panamanian subjects' sera were consistent with histories of endemic exposure to VSV, as determined by virus neutralization assays. Significantly different binding to viral proteins was seen in the group of 80 SLEpatients compared with the normal control group and with the rheumatic disease control group, by a variety of measures. For example, most of the reactivity in the SLEpatient sera included binding to the internal viral matrix (M) and N proteins, while the reactivity in the normal control sera was mostly against the surface viral glycoprotein (G) protein alone or the N protein alone. Within this SLEpatient cohort, associations were found between binding to N protein and anti-Ro precipitins and between binding to M protein and anti-nuclear RNP autoantibody precipitins. CONCLUSION: The data are consistent with the original specific hypotheses of a relationship between 60-kd Ro autoantigenicity and VSV, as well as with the suggestion that a rhabdovirus may be important in SLE. They do not, however, make possible any conclusions concerning the role of rhabdoviruses in the development of SLE or of anti-Ro autoimmunity.
Authors: J G Routsias; M Sakarellos-Daitsiotis; E Detsikas; A G Tzioufas; C Sakarellos; H M Moutsopoulos Journal: Clin Exp Immunol Date: 1994-12 Impact factor: 4.330
Authors: R H Scofield; W D Dickey; K L Hardgrave; B R Neas; R M Horowitz; R A McArthur; A Fujisaku; M B Frank; J B Harley; A ] Fujisak A [corrected to Fujisaku Journal: Clin Exp Immunol Date: 1995-02 Impact factor: 4.330