RESUMEN
Sera from 619 HBsAg+ subjects living in eastern Sicily, consecutively collected from 1975-1985, were tested for markers of delta virus (HDV) infection: delta antigen (HDAg), antibodies to delta (anti-HDIg), and also for antibodies to HBcore of IgM type (anti-HBcIgM) and for the system HBe-anti-HBe. The subjects included 210 asymptomatic carriers, 238 patients with acute hepatitis and 171 patients with chronic liver disease. HDAg was not found in any of the samples. Anti-HD was found in 28/171 (16.3%) patients with chronic liver disease, in 13/210 (6%) asymptomatic HBsAg carriers and in 13/238 (5.4%) patients with acute hepatitis. None of our patients were drug addicts. One had a history of blood transfusion, and nine came from the same family unit. The prevalence of HDV infection in eastern Sicily is lower than in other areas of Sicily possibly because of the lower percentage of HBsAg carriers in the local population. Parenteral transmission of HDV does not seem to play a major role in our area, while the familial clustering suggests close body contact as an important way of spread.
Asunto(s)
Hepatitis D/epidemiología , Adolescente , Adulto , Anciano , Antígenos Virales/análisis , Portador Sano/inmunología , Femenino , Hepatitis/complicaciones , Anticuerpos Antihepatitis/análisis , Hepatitis D/complicaciones , Virus de la Hepatitis Delta/inmunología , Antígenos de Hepatitis delta , Humanos , Hepatopatías/complicaciones , Masculino , Persona de Mediana Edad , SiciliaRESUMEN
Huntington's Disease (HD) is a degenerative neurological disorder with autosomal dominant transmission. Although immunological defect(s) have been postulated, no confirmed laboratory evidence for this exists. In the present study we observed activated T cells in the peripheral blood of HD patients (using 4F2 monoclonal antibody), whereas the percentage of T cells bearing T-cell activation markers such as HLA-DR and MLR4 antigens was normal. We then studied T cells of HD patients in some functional assays. Since it has been suggested that autologous mixed lymphocyte reaction (AMLR) includes several immune mechanisms in which distinct cell subsets interact and perform distinct regulatory functions, it is conceivable that the remarkable deficiency of AMLR herein observed in HD patients results from some abnormal immune regulation which may contribute to the pathology of this condition. Additional experiments demonstrated a defect of AMLR in three asymptomatic young sibs of HD patients, and coculture experiments between T cells of patients (as responders) and non-T cells of their sibs (as stimulators), and vice versa, produced no proliferative response. Subnormal responsiveness in allogeneic MLR was also observed. Normal or enhanced PHA-induced production of both IL-2 and IFN-gamma in vitro was detected. These experimental data suggest a cellular branch of the immune system in HD; however, they do not indicate if this defect is primary or secondary to the disease itself.