Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.

Hepatitis C virus (HCV) infected patients with vasculitis are often treated with the B-cell-depleting anti-CD20 antibody rituximab. Treatment reduces the cryoglobulins that cause vasculitis, yet it also leads to a transient increase in liver enzymes and HCV genomic RNA in the periphery. The mechanism underlying the increased viral load is unclear and both direct and indirect roles have been proposed for B cells in HCV infection. We previously reported that HCV can associate with B cells and can trans-infect hepatocytes. We established an in vitro assay to study the effect(s) of rituximab on B cell-associated HCV infectivity. Rituximab-mediated lysis of B cells in vitro increases the level of infectious HCV released from B cells. Our results, using a model where virus does not replicate in B cells, recapitulate observations seen in patients and may explain in part the rapid increase in blood HCV RNA observed after rituximab treatment.

Original publication

DOI

10.1371/journal.pone.0025789

Type

Journal article

Journal

PLoS One

Publication Date

2011

Volume

6

Keywords

Antibodies, Monoclonal, Murine-Derived, Antigens, CD20, B-Lymphocytes, Hepatitis C, Hepatocytes, Humans, Immunologic Factors, In Vitro Techniques, Interleukin-2, Killer Cells, Natural, Leukocytes, Mononuclear, Models, Biological, Models, Statistical, Rituximab