Figures
Hepatitis C virus inhibits NF-κB p65 in an infected liver.
HCV was used to infect mice with chimeric mouse/human livers, and resulted in inflammation and signs of hepatocyte damage in the absence of an adaptive immune system. Further examination found that apoptosis was restricted to infected human liver cells and was due to induction of stress and pro-apoptotic BAX combined with repression of anti-apoptotic NF-κB and BCL-xL. This image shows an HCV-infected liver with decreased levels of NF-κB p65 (green) in HCV-infected (red) cells (see Joyce et al., doi:10.1371/journal.ppat.1000291).
Image Credit: Michael A. Joyce, University of Alberta.
Citation: (2009) PLoS Pathogens Issue Image | Vol. 5(2) February 2009. PLoS Pathog 5(2): ev05.i02. https://doi.org/10.1371/image.ppat.v05.i02
Published: February 27, 2009
Copyright: © 2009 Michael A. Joyce. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
HCV was used to infect mice with chimeric mouse/human livers, and resulted in inflammation and signs of hepatocyte damage in the absence of an adaptive immune system. Further examination found that apoptosis was restricted to infected human liver cells and was due to induction of stress and pro-apoptotic BAX combined with repression of anti-apoptotic NF-κB and BCL-xL. This image shows an HCV-infected liver with decreased levels of NF-κB p65 (green) in HCV-infected (red) cells (see Joyce et al., doi:10.1371/journal.ppat.1000291).
Image Credit: Michael A. Joyce, University of Alberta.