Washington: A research has found the mechanism behind the establishment and maintenance of persistent infection by Hepatitis B virus (HBV). It could help in the development of new therapeutic strategies.
The research has been published in the PLOS journal.
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 anti-viral 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 study, researchers examined the mechanisms underlying the expansion of myeloid-derived suppressor cells (MDSCs) and the suppression of T-cell responses in persistent HBV infection.
The researchers analysed 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 favours the establishment of persistent HBV infection. The HBeAg-MDSC-IDO axis may, therefore, serve as an immunotherapeutic target of chronic hepatitis B.
“HBV has many 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,” said the authors.
[source_without_link]ANI[/source_without_link]