To characterize patients with mumps vaccine failure, avidity testing was performed with the Enzygnost Anti-Parotitis Virus/IgG kit using a single-dilution–6 M urea denaturation method. Five groups of patients were tested. Group 1 consisted of 29 patients with primary mumps infections; group 2 was 20 children and adults with a definite history of natural infection; group 3 was 7 patients with a recent mumps vaccination, 1 of whom developed parotid gland swelling and aseptic meningitis; group 4 was 14 patients with mumps vaccine failure; and group 5 was 6 patients with recurrent episodes of parotitis in addition to a history of vaccination. On the basis of the results of groups 1 and 2, an avidity of ≦31% was determined to be low, and ≧32% was determined to be high. Avidity maturation from low to high appears to occur around 180 days after the acute illness. The results of group 3 showed that the vaccine-induced immunoglobulin G (IgG) had very low avidity. Among the 14 patients in group 4, 12 patients, including 7 with a positive IgM response, were diagnosed as having secondary vaccine failures. The results of group 5 suggested the possibility that the avidity of the mumps vaccine-induced IgG remains low or borderline. These results showed that secondary mumps vaccine failure occurs not infrequently, even among school age children under condition in which the vaccine coverage is low (i.e., 33% in our study population), and therefore, vaccinees are prone to be exposed to wild-type viruses. Avidity testing should provide information useful for the analysis of mumps virus infections.

Nephrotic syndrome developed in two children who carried hepatitis B virus. Both their serums contained hepatitis B surface antigen and hepatitis B e antigen (HBeAg). Two physicochemically and immunologically different categories of HBeAg activity were identified in their serums--i.e., small molecular (free) and large molecular (associated with IgG). Their kidney-biopsy specimens disclosed pathologic changes typical of membranous glomerulonephritis. By a fluorescent-antibody technic, HBeAg was found to be deposited in diffuse granular fashion, along glomerular capillary walls together with IgG and beta1C, but no deposition of hepatitis B surface antigen was detected. The presence of HBeAg in association with IgG both in the serum and in the kidneys of these patients suggests that HBeAg caused membranous glomerulonephritis by inducing the formation and deposition of immune complexes.

SUMMARY:Macrophage migration inhibitory factor (MIF) was the first lymphokine identified in activated T-lymphocytes. MIF can induce proinflammatory cytokines, such as interleukin-1 and tumor necrosis factor-(~. In this study, we identified MIF expression in a tissue specimen of a normal portion of a nephrectomized human kidney by reverse transcription-polymerase chain reaction (RT-PCR) and Westem blot analysis. Furthermore, immunohistochemical study using an anti-human MIF polyclonal antibody demonstrated that MIF was mostly present in the renal tubule epithelial cells and, to a lesser extent, in Bowman's capsular epithelial cells. We also carried out immunohistochemistry on cultured human renal proximal tubule epithelial cells, which showed that MIF was present in the cytoplasm of the epithelial cells. These results suggest the possibility that MIF takes part in the mechanism of inflammation and immunological events in the human kidney:

No abstract