The Role of Fc Gamma RIIb Expression in Chronic Hepatitis B Virus Infection

Hepatitis B virus blood test, conceptual image.
Researchers conducted a study to determine the association between Fc gamma RIIb expression concentrations and chronic hepatitis B virus infection progression.

Fc gamma receptor IIb (FcgRIIb) levels were associated with progression of liver inflammation and fibrosis in patients with chronic hepatitis B virus (CHBV) infection, according to results of a study published in BMC Infectious Diseases.

Patients (n=55) with CHBV infection, HBV carriers (n=64), and healthy controls (n=24) were recruited for this study from the First Hospital of Jilin University in China between 2015 and 2020. The researchers used an enzyme-linked immunosorbent assay to measure patients’ serum FcgRIIb concentrations. They also employed an immunohistochemical method to identify FcgRIIb expression in liver biopsy specimens from patients with CHBV infection.

Among patients in the CHBV, HBV carrier, and control cohorts, the mean (SD) ages were 40.6 ± 11.4, 41.2 ± 11.8, and 46.0 ± 12.3 years, and 29.1%, 40.6%, and 58.3% were women, respectively. Among patients in the CHBV and HBV carrier cohorts, 25.5% and 65.6% were HBV e antigen negative (P <.001) and they had a mean of 6.1 ± 1.9 and 4.4 ± 2.5 HBV-DNA log10 copies/ml, respectively (P <.001).

The researchers found that serum FcgRIIb concentrations were most increased among patients in the control cohort (201.9 ± 15.19 ng/ml), followed by those in the HBV carrier cohort (183.9 ± 33.47 ng/ml), and then those in the CHBV cohort (141.0 ± 37.14 ng/ml). Patients in the CHBV cohort had significantly decreased serum FcgRIIb concentrations compared with both those in the control (P <.001) and HBV carrier cohorts (P =.007). Of note, Patients in the HBV Carrier and control cohorts did not differ significantly (P =.123). After stratification by HBV e antigen status, patients who were positive for the antigen had significantly decreased serum FcgRIIb concentrations compared with those who were negative for the HBV e antigen (P =.007).

The researchers noted that concentrations of serum FcgRIIb were negatively correlated with concentrations of both aspartate aminotransferase (AST; r, -0.3936; P =.0063) and alanine aminotransferase (ALT; r, -0.3459; P =.0097).

Among the 18 patients with CHBV infection who underwent liver biopsy, specimen analysis showed that 5 patients had severe CHBV, 4 had moderate CHBV, 5 had mild CHBV, and 4 had normal liver tissue. Of patients with normal liver tissue, as well as those with mild, moderate, and severe CHBV infection, the mean integrated optical density of FcgRIIb were 23,696 ± 3847.33, 21,392.93 ± 7536.20, 10,287.25 ± 2878.82, and 5214.78 ± 1071.27, respectively. Although serum FcgRIIb concentrations among patients with mild CHBV showed no significant differences compared with those with normal liver tissue, FcgRIIb concentrations were significantly decreased among those with moderate CHBV vs those with normal liver tissue (P =.006 vs P <.001, respectively). Of note, the researchers found that FcgRIIb concentrations tended to decrease in accordance with pathologic changes related to hepatitis.

On analysis of liver biopsy specimens, FcgRIIb expression concentrations were negatively correlated with AST (r, -0.69; P =.00), ALT (r, -0.69; P =.00), fibrosis grade (r, -0.91; P <.001), and inflammation stage (r, -0.88; P <.001); however, they were positively correlated with platelet count (r, 0.65; P =.00).

Serum FcgRIIb concentrations were found to be predictive of liver inflammation grade 4, with an area under the receiving operator characteristic curve (AUROC) of 0.98 (95% CI, 0.79-1.00), a sensitivity of 1.00, and a specificity of 0.92. For liver fibrosis stage 4, FcgRIIb had a predictive AUROC value of 0.93 (95% CI, 0.71-0.99) with a sensitivity of 1.00 and specificity of 0.93.

This study was limited by the small number of serum and liver tissue samples included in the analysis. In addition, the researchers noted the need to verify the study results with a validation cohort.

According to the researchers, “[this] research supports the conclusion that FcgRIIb [concentrations] are significantly related to [CHBV] infection and progression in [CHBV infection].” They concluded that, “changes in FcgRIIb may influence the progression of hepatic inflammation and fibrosis in patients [with CHBV infection].”


Jin J, Liu Y, Xu X, Wang Z, Niu J. The association between Fc gamma RIIb expression levels and chronic hepatitis B virus infection progression. BMC Infect Dis. 2021;21(1):1235. doi:10.1186/s12879-021-06918-7