Hepatitis: Feng G

Li M, Zhou Y, Feng G, Su SB. · Institute of Inflammation and Immune Diseases, Shantou University Medical College, Shantou 515041, China. · Curr Mol Med. · Pubmed #19355917 No free full text.

Abstract: Toll-like receptors (TLRs) form a large family of pattern recognition receptors with at least 11 members in human and 13 in mouse. TLRs recognize a wide variety of microbial components and potential host-derived agonists that have emerged as key mediators of innate immunity. TLR signaling also plays an important role in the activation of the adaptive immune system by inducing proinflammatory cytokines and upregulating costimulatory molecules of antigen presenting cells. The dysregulation of TLR signaling may cause autoimmunity. This review discusses the contribution of TLR signaling to the initiation and progression of autoimmune diseases, such as rheumatoid arthritis, experimental autoimmune encephalitis, myocarditis, hepatitis, kidney disease, systemic lupus erythematosus, diabetes, obesity, and experimental autoimmune uveitis as well as aging. The involvement of TLR signaling in the pathogenesis of autoimmune diseases may provide novel targets for the development of therapeutics.

Zhao L, Liu H, Zhu S, Feng G, Qi Z. · Department of Microbiology, Second Military Medical University, 200433, Shanghai, China. · Sci China C Life Sci. · Pubmed #19448994 No free full text.

Abstract: Since cell signal transduction plays an important role in disclosing the nature of human diseases, the pathogenesis of viruses may result from the disturbance of intracellular signal cascades caused by viral proteins. Hepatitis C virus (HCV) is a main causative agent of severe human liver disorders worldwide. So far, the mechanisms of HCV pathogenicity remain unclear. Envelope protein 2 (E2) of HCV is thought to be responsible for initiating virus attachment to host cells, which is a prerequisite of HCV infection. We assume that some early events of HCV pathogenic effects may result from the interaction of HCV E2 protein with its cellular receptor (human CD81), which could regulate cell proliferation and differentiation. To test this hypothesis, the effects of HCV E2 protein on MAPK/ERK pathway in Molt-4 and U937 cells with or without human CD81 expression were investigated. The results showed that HCV E2 protein could specifically activate the MAPK/ERK pathway, and such activation was inhibited by monoclonal antibodies against CD81 or HCV E2, serum antibodies from HCV infected patients, and upstream MEK1 inhibitor PD98059. Moreover, HCV E2-driven MAPK/ERK or downstream transcription factor Elk-1 activation was completely blocked in the presence of PD98059. These findings strongly suggest that the regulation of transmembrane signaling by HCV E2 protein via its receptor(s) on host cells might contribute to the development of HCV-related diseases.

Zhang L, Feng G, Qiao G. · Department of Infectious Diseases, 2nd Clinical College, China Medical University, Shenyang 110003. · Zhonghua Shi Yan He Lin Chuang Bing Du Xue Za Zhi. · Pubmed #12569758 No free full text.

Abstract: OBJECTIVE: To investigate virus interaction in HBV and HCV superinfection. METHODS: The changes of serum markers of 30 patients with HBV and HCV superinfetion were observed. Meanwhile, mutation of HBV precore region at nt 1,896 and the amount of TNF alpha and IL-6 in sera were also investigated. RESULTS: Compared with HBV or HCV single infection, positive rates of HBeAg, HBV DNA and HCV RNA in superinfectim were lower, positive rates of anti-HBe was higher, the average titers of HBsAg, anti-HBcIgG and anti-HCV were significantly lower, too. In some patients, HBsAg were seronegatively convested. Occurrence rate of HBV precore region mutation at nt1896 and levels of TNF alpha and IL-6 in sera were higher in super infection than those in single infection. CONCLUSION: Interference existed between HBV and HCV superinfection, conversion from HBeAg to anti-HBe was not only due to the suppression by HCV but also to the mutation of HBV precore region, and HCV may be a reason causing HBV precore region mutation through increasing the pressure of the body's immunosystem.