Clinical and laboratory aspects of raised virus antibody titres in systemic lupus erythematosus.

A possible role of virus infection in the pathogenesis of systemic lupus erythematosus (SLE) has been postulated.This concept has been supported by the demonstration by Mellors, Shirai, Aoki, Huebner, and Krawczynski (1971) and Levy and Pincus (1970) of a role of virus infection in the disease of New Zealand mice (NZB) which is a model of SLE (Howie and Helyer, 1968); by reports of microtubular struc- tures in glomerular endothelium from SLE patients (Fresco, 1968; Grausz, Earley, Stephens, Lee, and Hopper, 1970; and Norton, 1969) and by the occur- rence of high antibody titres to measles, rubella, and parainfluenza 1 viruses (Phillips and Christian, 1970; Hurd, Dowdle, Casey, and Ziff, 1972; Hollinger, Sharp, Lidsky, and Rawls, 1971; Feltkamp, van Loghem, Lucas, van der Noordaa, de Rooy, and ten Veen, 1971) in SLE patients as compared to controls.High antibody titres to the Epstein-Barr (EB) virus have also been reported by Dalldorf, Carvalho, Jamra, Frost, Erlich, and Marigo (1969), and in a larger survey of our own (Evans, Rothfield, and Niederman, 1971), to be present in SLE patients as compared to controls.The present study expands our previous preliminary communication on the increase of the four virus antibodies in SLE as compared to control