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
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