Late-onset rubella syndrome: coexistence of immune complex disease and defective cytotoxic effector cell function.
We studied a classical case of late-onset rubella syndrome characterized by multi-organ disease and persistence of live rubella virus in spite of high titres of specific antirubella antibodies and presence of large amounts of circulating immune complexes. When first studied at the age of 5 months there was a low proportion of T8+ lymphocytes. Functional studies revealed decreased activity of K and NK cells as well as alloreactive direct cytotoxic cells (CTL). Removal of cell-bound immunoglobulin and immune complexes tended to improve K and NK cell function in vitro. Plasma exchange transfusions carried out at 9 months of age resulted in clinical improvement. Normalization of cytotoxic effector cell functions and cessation of viremia accompanied recovery from active disease. The results indicate that defective cytotoxic effector cell function is the primary cause for the defective virus elimination in this syndrome.
D000914:Antibodies, Viral / Q000032:analysis; D000936:Antigen-Antibody Complex / Q000032:analysis; D005260:Female; D006801:Humans; D007105:Immune Complex Diseases / Q000150:complications*; D007136:Immunoglobulins / Q000032:analysis; D007231:Infant, Newborn; D007694:Killer Cells, Natural / Q000276:immunology*; D012409:Rubella / Q000150:complications / Q000276:immunology* / Q000382:microbiology; D012412:Rubella virus / Q000276:immunology; D013577:Syndrome; D013997:Time Factors
D000914:Antibodies, Viral; D000936:Antigen-Antibody Complex; D007136:Immunoglobulins