Hepatitis C virus and disrupted interferon signaling promote lymphoproliferation via type II CD95 and interleukins.

ABSTRACT:

Background & aims

The molecular mechanisms of lymphoproliferation associated with the disruption of interferon (IFN) signaling and chronic hepatitis C virus (HCV) infection are poorly understood. Lymphomas are extrahepatic manifestations of HCV infection; we sought to clarify the molecular mechanisms of these processes.

Methods

We established interferon regulatory factor-1-null (irf-1(-/-)) mice with inducible and persistent expression of HCV structural proteins (irf-1/CN2 mice). All the mice (n = 900) were observed for at least 600 days after Cre/loxP switching. Histologic analyses, as well as analyses of lymphoproliferation, sensitivity to Fas-induced apoptosis, colony formation, and cytokine production, were performed. Proteins associated with these processes were also as

SUBMITTER: Machida K 

PROVIDER: S-EPMC4197798 | biostudies-literature | 2009 Jul

REPOSITORIES: biostudies-literature