Publications by authors named "Silvia Sansonno"

Human enteroviruses (EVs) comprise >100 different types. Research suggests a non-chance association between EV infections and type 1 diabetes. Immunohistochemical studies with the anti-EV antibody 5D-8.

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Introduction: Hepatitis C virus (HCV) infection can be detected in virtually all patients with cryoglobulinemic vasculitis (CV). Among its many effects, the virus is able to stimulate the production of thymic stromal lymphopoietin (TSLP) by infected hepatocytes. In this study, we assessed the systemic levels and tissue distribution of TSLP in 60 chronically HCV-infected patients, 36 with and 24 without CV.

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Introduction: In hepatitis C virus (HCV)-related mixed cryoglobulinemia (MCG), the nonenveloped HCV core protein (HCV-Cp) is a constituent of the characteristic cold-precipitating immune complexes (ICs). A possible correlation between HCV-Cp, virologic, laboratory, and clinical parameters in both untreated MCG patients and those undergoing specific treatment was explored.

Methods: HCV-Cp was quantified by a fully automated immune assay.

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This study illustrates the use and efficacy of a combination of pegylated interferon-alpha (Peg-IFN-alpha) and ribavirin (RBV), with or without rituximab (RTX), in hepatitis C virus (HCV)-related mixed cryoglobulinemia (MC). Twenty-two patients with HCV-related MC received Peg-IFN-alpha (2a: 180 mug or 2b: 1.5 mug/kg) weekly plus RBV (1000 or 1200 mg) daily for 48 weeks, and RTX (375 mg/m(2)) once a week for 1 month followed by two 5-monthly infusions (termed PIRR).

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Persistent HCV infection may be associated with extrahepatic manifestations such as type II mixed cryoglobulinemia (II-MC), a clonal B cell proliferative disorder. In persistent HCV infection without II-MC, an increase in serum immunoglobulins (Ig) is commonly observed. This increase is polyclonal and is determined primarily by increased levels of IgG which include both HCV-specific and nonspecific antibodies.

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In addition to cause acute and chronic liver disease, hepatitis C virus (HCV) infection is frequently associated to autoimmune disorders, such as mixed cryoglobulinemia, primary glomerulonephritis, monoclonal gammopathy of undetermined significance and post-transplant proliferative disorders. Progression to malignant phenotype of B cells may be the consequence of additional genetic events or abnormal conditions resulting from modification of host cell genes involved in the control of oncogenes and oncoproteins. In this review, we will address the potential immune disregulatory mechanism(s) underlying HCV persistence.

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The diffuse large B-cell lymphoma (DLBCL) is the most common type of lymphoid cancer. The classical chemotherapy regimen given to these patients was the CHOP (Cyclophosphamide, Hydroxydaunorubicin or Adriamycin, Oncovin or Vincristine, Prednisone or Prednisolone), but recently rituximab with CHOP (R-CHOP) increased the number of cases responding to first line therapy. DLBCL classification identified three principle subgroups.

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