Type C RNA virus expression in systemic lupus erythematosus. New Zealand mouse model and human disease

Abstract

An antigen recognized by antisera produced against p30 (core) proteins of the four chief groups of mammalian type C viruses (murine, feline, RD-114 related to endogenous primate, and infectious primate group) is located in an immune-complex pattern in some renal glomeruli of human SLE patients with lupus proliferative glomerulonephritis but is not detected in normal or pathological control human kidneys. This antigen crossreacts with p30 interspecies determinants shared by the four chief virus groups and cross-reacts with a partially purified antigen extracted from human SLE spleen. The human SLE spleen antigen cross-reacts with p30 group antigen of RD-114 virus but not of feline or murine viruses. Some host immunoglobulins eluted from a human SLE kidney by acid-buffer show antibody-like activity against p30 group antigen of RD-114 virus but not of simian, feline, or murine viruses.The evidence that an endogenous type C virus is involved in murine SLE can be briefly summarized as

Identification of anaplasmataceae (haemobartonella) antigen and antibodies in systemic lupus erythematosus

“…Exogenous agents reported previously in association with SLE have included tubercle bacilli, streptococci, viruses, mycoplasmas, Haemobartonellae, tubular myxovirus structures, and type C viruses (1,13). However, the etiology of lupus remains unproved.…”

Type C RNA virus-specific antibody in human systemic lupus erythematosus demonstrated by enzymoimmunoassay.

“…The starting materials were human renal tissues obtained at postmortem examination of three patients with SLE described elsewhere (1,2). Briefly summarized, the duration of the disease in patients 1 and 2 was %/2 and 2 years, respectively; the SLE was associated with diffuse proliferative glomerulonephritis and showed typical glomerular deposits of host Ig and, less extensively, of type C viral p30-like antigen; the duration of the disease in patient 3 was 15 years; the SLE was not associated' with proliferative-type glomerulonephritis and showed glomerular deposits of host Ig but no detectable p30-like antigen.…”

“…Human systemic lupus erythematosus (SLE) is a multisystemic autoimmune syndrome of unknown etiology and multifactorial pathogenesis. Postmortem study of a subset of systemic lupus associated with proliferative glomerulonephritis has shown that an antigen related to the interspecies determinants of mammalian type C RNA viral core (p30) proteins is located in the renal glomerular lesions with human immunoglobulins (Igs) in an immune-complex pattern of deposition (1,2). We attempt to extend this finding by examining the immune deposits for the presence of a type C virus antibody.…”