Cytotoxic T lymphocytes and CD4 epitope mutations in the pre-core/core region of hepatitis B virus in chronic hepatitis B carriers in Northeast Iran

2017 ◽  
Vol 36 (4) ◽  
pp. 253-257 ◽  
Author(s):  
Sareh Zhand ◽  
Alijan Tabarraei ◽  
Amineh Nazari ◽  
Abdolvahab Moradi
2020 ◽  
Author(s):  
Xia Li ◽  
Chao Liu ◽  
Gui-Yu Li ◽  
Jie Mu ◽  
Lu-Shuang Xie ◽  
...  

Abstract Background: Viral hepatitis is still a major health problem in the world, such as chronic hepatitis B(CHB). Hepatitis B virus (HBV) easily causes liver cirrhosis and hepatocellular carcinoma that seriously endanger human health. However, the cellar and molecular pathology of hepatitis B virus is still unclear. Currently, the level of immunity and the inflammatory response are recognized as close relationship with the prognosis of CHB. Methods: Peripheral blood samples from 36 CHB patients and 14 healthy volunteers as control subjects in this study. We studied the change of T lymphocytes and the proteins levels of HMGB1-PTEN pathway in the CHB patients and the healthy controls by Flow cytometry and enzyme-linked immunosorbent assay (Elisa), and then further analyzed the correlation between T lymphocytes and HMGB1-PTEN pathway by constructing multiple regression equation and Pearson test. Results: The percentages of CD4+T, CD8+T cells in CHB patients were lower than those of the healthy controls, and the percentages of Th17, Treg, ratio of Th17/Treg and Tfh cells in CHB patients were higher than those of the healthy controls (P<0.01). HMGB1, PI3K, PDK1, Akt proteins in CHB patients were higher than healthy people (P<0.01). Furthermore, HMGB1-PTEN pathway proteins were negatively correlated with CD4+T, CD8+T cells, and positively correlated with Th17, Treg cells. Conclusions: Long term HBV infection could lead to decrease of immune function and activation of inflammatory response, which makes it difficult to cure chronic hepatitis B.


1991 ◽  
Vol 88 (6) ◽  
pp. 1793-1801 ◽  
Author(s):  
T Wakita ◽  
S Kakumu ◽  
M Shibata ◽  
K Yoshioka ◽  
Y Ito ◽  
...  

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