Literature DB >> 29731897

Hepatitis B virus inhibits the expression of complement C3 and C4, in vitro and in vivo.

Chengliang Zhu1, Hui Song2, Fengxia Xu2, Wei Yi1, Fang Liu3, Xinghui Liu2.   

Abstract

The immune system serves an important function in Hepatitis B virus (HBV) infection, and the complement system is a major component of innate immunity. However, the regulatory effect of HBV on complement proteins has not yet been fully elucidated. The present study focused on investigating the impact of HBV on the expression of complement proteins C3 and C4. A total of 226 patients with a clinical diagnosis of HBV infection were enrolled in the study, including 153 with chronic hepatitis B (CHB) and 73 with hepatocellular carcinoma (HCC), whereas 116 healthy individuals were included as a control group. Immunoturbidimetric detection was performed to determine the levels of complement C3 and C4 in the serum of the patients with HBV and the control group. The results revealed that the mean ± standard deviation C3 and C4 content was 1.223±0.237 and 0.226±0.052 g/l for the control group, 0.687±0.150 and 0.145±0.070 g/l for the patients with CHB, and 0.829±0.332 and 0.174±0.088 g/l for the patients with HCC, respectively. The levels of complement C3 and C4 in the patients with CHB or HCC were significantly lower than the control group (P<0.05). The HBV infectious clone pHBV1.3 was used to transfect Huh7 cells; Huh7 cells transfected with the pBlue-ks empty vector were used as the blank control. The changes in mRNA and protein expression of complements C3 and C4 were detected by RT-PCR and western blotting. When compared with the control cells, the Huh7 cells transfected with pHBV1.3 exhibited reduced C3 and C4 mRNA and protein expression levels. It was concluded that HBV can inhibit the expression of complement C3 and C4 in vitro and in vivo, which may lay the foundation for revealing the pathogenesis of HBV.

Entities:  

Keywords:  complement C3; complement C4; expression; hepatitis B virus; innate immunity

Year:  2018        PMID: 29731897      PMCID: PMC5920570          DOI: 10.3892/ol.2018.8223

Source DB:  PubMed          Journal:  Oncol Lett        ISSN: 1792-1074            Impact factor:   2.967


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