Sera of patients with systemic lupus erythematosus(SLE) showed significantly higher complement fixation reactivities with 8 of 10 virus antigen preparations compared to sera of normal subjects, including virus workers, confirming earlier observations. However, one-third of SLE sera were also reactive with cellular antigens, prepared in a manner identical to viral antigens, but from cells not infected with virus. By contrast, only one of 49 normal sera showed reactivity with one of nine cellular antigens, at a minimal titer. Apparently heightened reactivities of SLE sera with virus antigens could be explained in many instances on the basis of reactions with cellular antigens. Serum reactivities with nonviral tissue antigens in SLE must be considered in interpretation of immunologic studies related to viruses and SLE.High levels of a wide spectrum of unusual antibodies reactive with proteins and nucleic acids are found in sera of patients with systemic lupus erythematosus (SLE) (1). Considerable attention has been directed toward possible disorders of immunologic regulation and/ or atypical virus infection in the etiology of these antibodies (2). Identification of virus-associated microtubular structures in electron micrographs (3-5) and elevated antibody titers to a number of viruses (6-12) have heightened interest in the virus hypothesis in SLE (l3,14). In studies reported here, the finding of raised antibody titers to many virus antigen preparations in sera of SLE patients compared to sera of normal subjects, including virus workers, has been confirmed. Certain SLE sera showed levels of complement fixing reactivity far greater than those seen in any of the normal sera tested. However, unusual reactivities with control antigen preparations, i.e. replicate cell cultures used to prepare virus antigens that had not been infected with viruses, have also been found in over one-third of SLE sera. Reactivities with control antigen preparations, which are not found in normal sera, substantially complicate analysis of viral imrnunodiagnostic studies involving sera of SLE patients.
PATIENTS AND METHODSSera. Two study groups of sera were collected from SLE patients who fulfilled clinical criteria described in previous reports (l5), along with matched control sera. Male SLE patients were excluded from the studies because too few were available for meaningful analysis. To establish the first (study) group, sera were collected from 50 female SLE patients; 13 showed anticomplementary activity and were not further