J Biomed Sci. 2018 Jul 28;25(1):59. doi: 10.1186/s12929-018-0460-2.
The human C-type lectin 18 is a potential biomarker in patients with chronic hepatitis B virus infection.
Tsai TY1,2, Peng CY2,3, Yang HI4, Huang YL4, Tao MH5, Yuan SS6, Lai HC2, Hsieh SL7,8,9.
Author information
1
Ph.D. Program for Translational Medicine, China Medical University and Academia Sinica, Taichung and Taipei, Taiwan.
2
Division of Hepatogastroenterology, Department of Internal Medicine, China Medical University Hospital, 2, Yude St., North District, Taichung, 404, Taiwan.
3
School of Medicine, China Medical University, Taichung, Taiwan.
4
Genomics Research Center, Academia Sinica, 128, Academia Road, Sec. 2, Nankang District, Taipei, 115, Taiwan.
5
Institute of Biomedical Sciences, Academia Sinica, 128, Academia Road, Sec. 2, Nankang District, Taipei, 115, Taiwan.
6
Institute of Statistical Sciences, Academia Sinica, 128, Academia Road, Sec. 2, Nankang District, Taipei, 115, Taiwan.
7
Genomics Research Center, Academia Sinica, 128, Academia Road, Sec. 2, Nankang District, Taipei, 115, Taiwan. [email protected].
8
Institute of Clinical Medicine, National Yang-Ming University, Taipei, Taiwan. [email protected].
9
Department of Medical Research, Taipei Veterans General Hospital, Taipei, Taiwan. [email protected].
Abstract
BACKGROUND:
Hepatitis B virus (HBV) infection is a common disease worldwide and is known to cause liver disease. C-type lectin 18 (CLEC18) is a novel secretory lectin highly expressed in human hepatocytes. Because the liver is the major target of HBV infection, we investigated whether the expression of CLEC18 can be used as a biomarker for HBV infection.
METHODS:
The expression level of CLEC18 in human liver chimeric mice with/without HBV infection was measured by quantitative real time polymerase chain reaction (qPCR) assay. Baseline plasma CLEC18 levels in 271 treatment-naive patients with chronic hepatitis B (CHB) undergoing nucleos(t)ide analogue (NUC) therapy and 35 healthy donors were measured by enzyme-linked immunosorbent assay, and the relationships to other clinical data were analyzed.
RESULTS:
The expression of CLEC18 was down-regulated in the human liver chimeric mice after HBV infection. Plasma CLEC18 levels were lower in the patients with CHB compared to the healthy donors and positively correlated with HBV DNA and HBsAg levels (P < 0.05). Multivariate Cox proportional hazard regression analysis identified a baseline plasma CLEC18 level of 320-2000 pg/mL to be an independent predictor of HBeAg loss (hazard ratio (HR): 2.077, P = 0.0318), seroconversion (HR: 2.041, P = 0.0445) and virological response (HR: 1.850, P = 0.0184) in 101 HBeAg-positive patients with CHB undergoing NUC therapy.
CONCLUSIONS:
Plasma CLEC18 levels were correlated with the stage of HBV infection and could predict HBeAg loss and seroconversion in the patients with CHB undergoing NUC therapy.
KEYWORDS:
C-type lectin 18; HBeAg seroconversion; Hepatitis B virus