Copy number gain of pro-inflammatory genes in patients with HBV-related acute-on-chronic liver failure.

ABSTRACT:

Background

Host genetic factors such as single nucleotide variations may play a crucial role in the onset and progression of HBV-related acute-on-chronic liver failure (ACLF). However, the underlying genomic copy number variations (CNVs) involved in the pathology are currently unclear.

Methods

We genotyped two cohorts with 389 HBV-related ACLF patients and 391 asymptomatic HBV carriers (AsCs), and then carried out CNV-based global burden analysis and a genome-wide association study (GWAS).

Results

For 1874 rare CNVs, HBV-related ACLF patients exhibited a high burden of deletion segments with a size of 100-200 kb (P value = 0.04), and the related genes were significantly enriched in leukocyte transendothelial migration pathway (P value = 4.68 × 10^-3). For 35

SUBMITTER: Sun F 

PROVIDER: S-EPMC7709420 | biostudies-literature | 2020 Dec

REPOSITORIES: biostudies-literature