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Mechanism of Persistent Infection Caused by Hepatitis B Virus Identified

by Ramya Rachamanti on April 19, 2019 at 12:19 PM
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Mechanism of Persistent Infection Caused by Hepatitis B Virus Identified

New study identified how a hepatitis B viral protein stimulates the expansion of immune cells which impair antiviral responses, published in the open-access journal PLOS Pathogens by Haitao Guo of the Indiana University School of Medicine, Bin Wang and Jiming Zhang of Fudan University, and colleagues.

Their findings explain how the hepatitis B virus (HBV) establishes and maintains chronic infection, and could lead to the development of novel therapeutic strategies.

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HBV is a blood-borne pathogen that chronically infects approximately 350 million people worldwide, and more than 780,000 patients die annually due to HBV-related liver diseases. Chronic HBV infection is associated with impaired virus-specific T-cell responses.

Myeloid-derived suppressor cells (MDSCs) are immune cells known to play a critical role in impairing antiviral T-cell responses. In addition, the hepatitis B e-antigen (HBeAg) - a hepatitis B viral protein -- may represent a viral strategy to establish persistent infection, but the mechanism remains largely unknown. In the new study, the researchers examined the mechanisms underlying the expansion of MDSCs and the suppression of T-cell responses in persistent HBV infection.
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The researchers analyzed the circulation frequency of MDSCs in 164 patients with chronic HBV infection and 70 healthy donors. They found that the frequency of circulating MDSCs in HBeAg-positive patients is higher than in HBeAg-negative patients.

Moreover, HBeAg induced the expansion of MDSCs through the upregulation of a molecule called indoleamine-2, 3-dioxygenase (IDO), which plays a critical role in the suppression of T-cell proliferation.

According to the authors, the findings suggest a novel mechanism in which HBeAg-induced MDSC expansion impairs T-cell function through the IDO pathway and favors the establishment of persistent HBV infection. The HBeAg-MDSC-IDO axis may therefore serve as an immunotherapeutic target of chronic hepatitis B.

The authors add, "HBV has may tricks to mess up the host immune system for maintaining a persistent infection, HBeAg is one of the culprits. Breaking the HBeAg-IDO-MDSC nexus may hold promise for developing new HBV therapeutics to treat HBeAg-positive patients."



Source: Eurekalert
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