In present study, the whole-genome sequencing of HBV isolated from twelve CHB-M patients and twelve agematched ACLF patients was conducted, and the mutations of HBV related to ACLF were screened by Illumina high-throughput sequencing. In L-690,330 addition, an independent case-control study with 438 cases was carried out to verify the association between the newly identified mutations in HBV genome and serious hepatitis B by direct sequencing. Up to now, many antiviral drugs, such as lamivudine, adefovir, Tenofovirand entecavir, have been used to treat hepatitis B, and one of the key issues for preventing the development of ACLF is early antiviral treatment of chronic hepatitis B with acute exacerbation. So it is Lestaurtinib important for us to find some viral biomarkers related to hepatitis B progression and to diagnose ACLF as early as possible. The results of Illumina high-throughput sequencing in present study indicated that there were significant differences of the mutations at seven sites of HBV between twelve ACLF cases and twelve CHB-M cases. Of these seven mutations, A1846T/G, G1896A and C1913A/G were studied extensively, whereas T216C, G285A, A2159G, and A2189C were novel ACLF-related mutations identified in this study. To verify the association between the newly identified mutations of HBV and ACLF, we carried out a case control study on 80 cases with ASC, 152 cases with CHB, 102 cases with CHB-s and 104 cases with ACLF. As HBV mutations may consecutively increase with aging and the severe hepatitis are more frequent in men than in women, we adjusted the age and sex in evaluating the association of seven mutations with ASC, CHB-M, CHB-S, or ACLF. It was found that in the subjects with genotype B, the mutations at nt.216, nt.285, nt.1896, and nt.1913 sites were significantly related to CHB-S or ACLF as compared to ASC; the mutations at nt.2159 and nt.2189 sites were significantly associated with ACLF as compared to CHB-S. The hippocampus may be a highly relevant brain structure, given the widely reported associations among childhood trauma, dysregulated physiological and emotional stress responses, and structural changes in the hippocampus in stress-related disorders. Current neurobiological theories of MDD postulate that altered serotonin neurotransmission may represent a biological risk factor, which is more likely to be expressed in the presence of adversity. Consistent with this model, researchers have identified a number of 5-HT polymorphic genes that may increase the risk of developing a mental disorder.