What is it about?
The hepatitis B virus (HBV) is an intracellular pathogen that relies on the host cell's metabolism to reproduce. Researchers conducted a study to investigate whether HBV affects host cell metabolism to support its reproduction. This study identified pyruvate kinase isoform M2 (PKM2), a key regulator of glucose metabolism, as a binding partner of viral surface antigens. We have found that the expression of viral surface antigens led to increased glucose consumption and lactate production, a phenomenon known as aerobic glycolysis, and reduced PKM2 activity in hepatocytes. Additionally, chemical activators of PKM2 reduced viral antigen expression, and reducing glycolysis also decreased viral surface antigen expression.
Featured Image
Why is it important?
Our findings suggest that HBV-induced metabolic changes may support its own reproduction and contribute to oncogenesis. Targeting glucose metabolism may be a potential strategy to restrain viral protein synthesis and subsequent oncogenesis in chronic HBV infection. In addition, this study also highlights the potential of PKM2 as a therapeutic target for HBV treatment.
Perspectives
We believe the most important message of this study is the finding that reducing glucose metabolism can work to restrain viral protein synthesis and subsequent oncogenesis in chronic HBV infection. This study provides new insights into the complex interactions between HBV and host cell metabolism. Accordingly, controlling glucose metabolism or modulating PKM2 activity may be considered a prophylactic approach to prevent the HBV-mediated development of liver cancer.
Lily Wang
National Tsing Hua University
Read the Original
This page is a summary of: Aerobic glycolysis supports hepatitis B virus protein synthesis through interaction between viral surface antigen and pyruvate kinase isoform M2, PLoS Pathogens, March 2021, PLOS,
DOI: 10.1371/journal.ppat.1008866.
You can read the full text:
Contributors
The following have contributed to this page
