Animals ; Antigens, CD ; metabolism ; Hepacivirus ; pathogenicity ; physiology ; Humans ; Receptors, LDL ; physiology ; Receptors, Virus ; physiology ; Tetraspanin 28

Animals ; Antigens, CD ; metabolism ; CHO Cells ; Cricetinae ; Cricetulus ; Endocytosis ; Hepacivirus ; genetics ; pathogenicity ; physiology ; Tetraspanin 28 ; Viral Envelope Proteins ; genetics

Antigens, CD ; chemistry ; physiology ; Hepacivirus ; physiology ; Humans ; Membrane Proteins ; chemistry ; physiology ; Receptors, LDL ; chemistry ; physiology ; Receptors, Virus ; chemistry ; physiology ; Tetraspanin 28

Antigens, CD ; physiology ; Dendritic Cells ; physiology ; Hepatitis C, Chronic ; etiology ; immunology ; virology ; Histocompatibility Antigens Class II ; physiology ; Humans ; Membrane Proteins ; physiology ; Signal Transduction ; Tetraspanin 28 ; Viral Nonstructural Proteins ; physiology

OBJECTIVE: To determine the role of miR-155 in the pathogenesis of generalized myasthenia gravis (GMG) and the effect of dexamethasone (DXM) on miR-155. METHODS: The expression of miR-155 in B cells from the GMG patients and healthy controls was analyzed by qPCR. The B cells were cultured with DXM and PBS. The B cell proliferation was examined by MTT; CD80 and CD86 frequencies were detected by flow cytometry; and anti-AChRIgG and isotypes anti-AChR-IgG1, 2, 3 in the supernatant were detected by ELISA. RESULTS: qPCR revealed that the expression of miR-155 in the B cells was much higher than that in the controls, and the miR155 expression decreased after DXM treatment. flow cytometry showed that there was no significant difference in the proliferation and the expressions of CD80 and CD86 in the B cells between the DXM group and the PBS group. The concentration of anti-AChR-IgG1 was obviously lower in the DXM group than in the PBS group, but the concentration of anti-AChRIgG, anti-AChR-IgG2, and anti-AchR-IgG3 was similar. CONCLUSION high expression of miR-155 may be associated with myasthenia gravis progression. DXM may disturb the antibody class switch of B cells by suppressing the expression of miR-155 and improve the symptom of MG patients.
Adult ; B-Lymphocytes ; cytology ; immunology ; metabolism ; B7-1 Antigen ; metabolism ; Cell Proliferation ; Cells, Cultured ; Dexamethasone ; therapeutic use ; Female ; Humans ; Immunoglobulin G ; immunology ; Male ; MicroRNAs ; genetics ; metabolism ; Middle Aged ; Myasthenia Gravis ; drug therapy ; genetics ; immunology ; Receptors, Cholinergic ; immunology ; Tetraspanin 28 ; metabolism ; Young Adult

Hepatitis C virus (HCV) is a positive sense, single-stranded RNA virus in the Flaviviridae family. It causes acute hepatitis with a high propensity for chronic infection. Chronic HCV infection can progress to severe liver disease including cirrhosis and hepatocellular carcinoma. In the last decade, our basic understanding of HCV virology and life cycle has advanced greatly with the development of HCV cell culture and replication systems. Our ability to treat HCV infection has also been improved with the combined use of interferon, ribavirin and small molecule inhibitors of the virally encoded NS3/4A protease, although better therapeutic options are needed with greater antiviral efficacy and less toxicity. In this article, we review various aspects of HCV life cycle including viral attachment, entry, fusion, viral RNA translation, posttranslational processing, HCV replication, viral assembly and release. Each of these steps provides potential targets for novel antiviral therapeutics to cure HCV infection and prevent the adverse consequences of progressive liver disease.
Antigens, CD81/metabolism ; Genome, Viral ; Hepacivirus/genetics/*physiology ; Humans ; RNA, Viral/metabolism ; Scavenger Receptors, Class B/metabolism ; Viral Envelope Proteins/chemistry/metabolism ; Viral Nonstructural Proteins/chemistry/metabolism ; Virus Assembly ; Virus Internalization ; Virus Replication