Abstract
The mechanisms by which HCV may cause an abnormal B cell expansion remain puzzling. A direct transforming role of the virus appears unlikely, considering 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 undergo mutational events that lead to the development of cryoglobulinemia or non-Hodgkin’s lymphoma. Numerous attempts have been made to unravel HCV-B cell interaction and define the nature of the HCV antigen, driving B cell disorders. Starting from a brief review of the pathophysiology of B cell activation, we discuss in detail functional and molecular evidences supporting or arguing against current directions in B cell biology during chronic HCV infection.
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Racanelli, V., Brunetti, C. (2012). B Cell Activation: General to HCV-Specific Considerations. In: Dammacco, F. (eds) HCV Infection and Cryoglobulinemia. Springer, Milano. https://doi.org/10.1007/978-88-470-1705-4_4
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DOI: https://doi.org/10.1007/978-88-470-1705-4_4
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