Recently, Plos Pathogens, a leading international journal in the field of virology, published the scientific research achievement of Professor Wei Haiming and Professor Tian Zhigang of the School of Life Sciences, University of Science and Technology of China, “TGF-β1 (TGF-β). Β1) downregulates NKG2D/DAP10 and 2B4/SAP expression, thereby reducing the ability of human natural killer cells to fight HBV." It reveals the long-standing molecular mechanism of the hepatitis B virus in escaping natural killer cells and thus in the human body. The first author of the article is Sun Cheng, a doctoral student at the School of Life Sciences, University of Science and Technology of China, and the authors are Wei Haiming and Tian Zhigang.
China is a major country infected with hepatitis B virus. About 120 million people are infected with hepatitis B virus. Mother-to-infant transmission is the main route of hepatitis B virus infection. Newborns can persist in the body for several years after infection, and can develop gradually after puberty. So far, it is not clear why hepatitis B virus evades the body's immune system and causes long-term survival in the body.
In this study, 154 cases of hepatitis B virus carriers and hepatitis B patients were studied for systemic immunology. It was found that the number of natural anti-virus cells, the number of natural killer cells, was significantly reduced in patients with persistent hepatitis B virus infection, and residual natural killer cells were difficult to be activated. The double-signaling molecules NKG2D/DAP10 and 2B4/SAP, which exert lethal effects on the virus, were significantly attenuated. Further analysis revealed that a large number of immunosuppressive factors, transforming growth factor β1 (TGF-β1), were present in the hepatitis B virus carrier. Factors can lead to cell cycle arrest of natural killer cells and thus loss of antiviral effect. Treatment with anti-transforming growth factor β1 antibody can restore the function of natural killer cells to a greater extent. This study is helpful for understanding the mechanism of long-term persistent infection of hepatitis B virus in humans. The research work is supported by the funding of the key projects of the State Fund Committee.
China is a major country infected with hepatitis B virus. About 120 million people are infected with hepatitis B virus. Mother-to-infant transmission is the main route of hepatitis B virus infection. Newborns can persist in the body for several years after infection, and can develop gradually after puberty. So far, it is not clear why hepatitis B virus evades the body's immune system and causes long-term survival in the body.
In this study, 154 cases of hepatitis B virus carriers and hepatitis B patients were studied for systemic immunology. It was found that the number of natural anti-virus cells, the number of natural killer cells, was significantly reduced in patients with persistent hepatitis B virus infection, and residual natural killer cells were difficult to be activated. The double-signaling molecules NKG2D/DAP10 and 2B4/SAP, which exert lethal effects on the virus, were significantly attenuated. Further analysis revealed that a large number of immunosuppressive factors, transforming growth factor β1 (TGF-β1), were present in the hepatitis B virus carrier. Factors can lead to cell cycle arrest of natural killer cells and thus loss of antiviral effect. Treatment with anti-transforming growth factor β1 antibody can restore the function of natural killer cells to a greater extent. This study is helpful for understanding the mechanism of long-term persistent infection of hepatitis B virus in humans. The research work is supported by the funding of the key projects of the State Fund Committee.
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