Titlebook: HCV Infection and Cryoglobulinemia; Franco Dammacco Book 20121st edition Springer-Verlag Italia 2012 Autoimmunity.Cryoglobulinemia.HCV.Imm

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https://doi.org/10.1007/978-3-031-55935-8ing that B cells are not direct targets for productive virus replication and that viral RNA sequences cannot be integrated in the host genome. The current speculation is that protracted stimulation either by the virus alone or by HCV-containing immune complexes expands clones of B cells, which may u

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coagulation

Martin Holland (Senior Lecturer)cular virology are greatly contributing to the advancement of knowledge in this field. Model systems for the study of HCV cell entry include HCV-like particles, HCV pseudoparticles, cell-culture-produced HCV, and the tupaia animal model. Following the identification of tetraspanin CD81 with the use

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https://doi.org/10.1007/978-1-349-13095-5 also invades and persists in cells of the immune system. The functional and pathological consequences of HCV lymphotropism have become increasingly recognized. Studies on HCV compartmentalization in patients with symptomatic or clinically silent (occult) HCV infections demonstrated viral replicatio

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https://doi.org/10.1007/978-1-349-26543-5 cold with diseases. One major point was that there was no evidence for a known disease in many patients with “mixed” cryoglobulins. Thus, the terminology “mixed essential cryoglobulinemia” became accepted. The discovery of HCV as the causative agent of mixed essential cryoglobulinemia allowed not o

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https://doi.org/10.1057/9781137376374l activities, complement mediates the disposal of immune complexes and the products of inflammatory injury. Accordingly, low levels of complement suggesting ongoing complement activation and consumption are a well-known phenomenon in patients with cryoglobulinemia. The consumption of complement comp

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