Abstract
ObjectiveThe results of studies on the relation between Mannose-binding lectin gene (mbl2) polymorphism and HBV infection were contradictory and inconclusive. In order to shed a light on these inconsistent findings and to clarify the role of mbl2 polymorphisms in susceptibility or progression of chronic hepatitis B (CHB), a meta-analysis was performed.MethodsPubMed and Embase were searched for available articles. A meta-analysis was performed to examine the association between mbl2 polymorphisms and chronicity or progression of hepatitis B infection. Odds ratio (OR) and its 95% confidence interval (CI) served as indexes.ResultsA total of 17 eligible studies were involved, including 2151 healthy controls (HC), 1293 spontaneous recovered (SR) patients with acute infection, 2337cases with chronic hepatitis B (CHB) and 554 cases with progressive hepatitis B. There was no evidence of significant association between mbl2 exon1 polymorphisms and CHB risk in any genetic model or pairwise comparisons when compared with HC group or SR group. In the stratified analysis of ethnic groups, also no obvious relation between mbl2 polymorphism and CHB risk was identified. There was still no significant association between the complete mbl2 genotypic profile (including both the exon1 and the promoter gene) polymorphisms and CHB risk, as compared with SR group. However, it was found that there was an association between the mbl2 AO/OO genotype and severe hepatitis B (SHB) or liver cirrhosis (LC) (LC vs. HC:OR=3.66, 95%CI, 2.38-5.63; SHB vs. HC, OR=3.88, 95%CI, 2.26–6.64), but there was no relationship between the mbl2 AO/OO genotype and hepatocellular carcinoma (HCC) (OR=1.26, 95%CI, 0.82-1.94).ConclusionThe present meta-analysis indicated that mbl2 exon1 polymorphisms might not significantly associate with chronicity of HBV infection, but might be significantly related to the progressive HBV such as SHB and LC.
Highlights
Hepatitis B virus (HBV) infection leads to a wide spectrum of clinical presentations from inapparent infection to self-limiting acute hepatitis, chronic infection, fulminant hepatic failure (FHF), liver cirrhosis (LC) and hepatocellular carcinoma (HCC) [1]
13 studies not related to polymorphisms or HBV were excluded
The mbl2 polymorphisms could result in the Mannose-binding lectin (MBL) deficiency among a certain percentage of human, which potentially increases susceptibility to infectious disease [29,30]
Summary
Hepatitis B virus (HBV) infection leads to a wide spectrum of clinical presentations from inapparent infection to self-limiting acute hepatitis, chronic infection, fulminant hepatic failure (FHF), liver cirrhosis (LC) and hepatocellular carcinoma (HCC) [1]. The mechanism for persistent and progressive HBV infection is still unclear, but host immune factors and genetic factors may play important roles [2]. Mannose-binding lectin (MBL) is an important constituent of the human innate immune system, which, as an acute-phase reactant, is secreted by the liver. MBL is a calcium-dependent C-type lectin with a structural analogy of complement component C1q. MBL can bind through multiple lectin domains to the carbohydrate moieties expressed on the surface of many microbial organisms, and activate macrophages and the complement system cascade [3]. It is reported that serum MBL play an important role in regulating the production of proinflammatory cytokines such as TNF-α, IL-6 and IL-1βby monocytes in response to microbial infection [4], may affect the inflammation severity or disease progression
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
