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Severity of glomerulonephritis induced in different strains of suckling mice by infection with lymphocytic choriomeningitis virus: Correlation with amounts of endogenous interferon and circulating immune complexes
Author(s) -
Woodrow D.,
Ronco P.,
Riviere Y.,
Moss J.,
Gresser I.,
Guillon J. C.,
MorelMaroger L.,
Sloper J. C.,
Verroust P.
Publication year - 1982
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.1711380404
Subject(s) - lymphocytic choriomeningitis , interferon , immune system , virus , glomerulonephritis , biology , immunofluorescence , immunology , rickettsia , virology , kidney , antibody , endocrinology , cd8
Renal lesions due to neonatal infection with lymphocytic choriomeningitis virus were studied in three different strains of mice known to produce different amounts of viral interferon. Very severe ultrastructural lesions similar to those induced by exogenous interferon were found as early as day 8 in C3H mice which produced the highest amount of interferon. Further studies could not be performed in these mice since all died by day 14. Balb/c mice produced the lowest amount of interferon and had very mild ultrastructural lesions. An intermediate pattern was found in Swiss mice. After 30 days of infection, severe immune complex type glomerulonephritis detectable by light microscopy and immunofluorescence was observed in Swiss mice whereas mild lesions only were found in Balb/c mice. Circulating immune complexes were present in both strains but in greater amounts in Swiss than Balb/c mice. These results suggest that two factors at least are important in the development of glomerulonephritis: interferon produced early in life and the load of circulating immune complexes.