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Hepatitis C (HCV) is infamous for its association with the development of liver cancer, also known as hepatocellular carcinoma (HCC). Yet, the virus appears to be less abundant, and to replicate less well, in cancerous tissue. Recent research suggests this could be linked to the downregulation of the gene TACSTD2 in malignant liver cells, or hepatocytes. TACSTD2 regulates two proteins essential for the entry of HCV into hepatocytes: claudin-1 (shown above in red, in the upper panels) and occludin (in red, lower panels). In the absence of TACSTD2 (right-hand panels), the normal distribution of these proteins along the membranes of the hepatocytes (shown in the left-hand panels, with cell nuclei in blue), is disrupted, and infection with HCV is reduced. TACSTD2 thus appears to play a key role in facilitating virus entry into hepatocytes, and studying how it operates should help develop our understanding of HCV infections.

Written by Emmanuelle Briolat

Emmanuelle Briolat

Writer

A researcher specialising in visual signals in Lepidoptera, camouflage and the effects of light pollution, Emmanuelle’s writing covers a range of topics, from biomedical research to children’s books about moth defences.

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• Image by Vandana Sekhar, Juraj Kabat and Patrizia Farci; Laboratory of Infectious Diseases and Biological Imaging Facility, NIAID, NIH
• Hepatic Pathogenesis Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA
• Image originally published under a Creative Commons Licence (BY 4.0)
• Research published in PLOS Pathogens, March 2018