Human endogenous retroviruses (HERV) comprise 8% of the human genome and can be classified into at least 31 families. Increased levels of transcripts from the W and H families of HERV have been observed in association with human diseases, such as multiple sclerosis and schizophrenia. Although HERV transcripts have been detected in many tissues and cell-types based on microarray and PCR studies, the extent of HERV expression in different cell-types and diseases state has been less comprehensively studied. We examined overall transcription of HERV, and particularly of HERV-W and HERV-H elements in human postmortem brain samples obtained from individuals with psychiatric diagnoses (n = 111) and healthy controls (n = 51) by analyzing publicly available RNA sequencing datasets. Sequence reads were aligned to prototypical sequences representing HERV, downloaded from Repbase. We reported a consistent expression (0.1~0.2% of mappable reads) of different HERV families across three regions of human brains. Spearman correlations revealed highly correlated expression levels between three brain regionsacross 475 consensus sequences. By mapping sequences that aligned to the consensus sequences of HERV-W and HERV-H families to individual loci on chromosome 7, more than 60 loci from each family were identified, part of which are being transcribed. The ERVWE1, locus located at chr7q21.2, exhibited high levels of transcription across the three datasets. Notably, we demonstrated a trend of increased expression of overall HERV, as well as HERV-W family in samples from both schizophrenia and bipolar disorder patients. The current analyses indicate that RNA sequencing is a useful approach for investigating global expression of repetitive elements, such as HERV, in the human genome. HERV-W/H with the tendency of transcription up-regulation in patients suggests potential implication of HERV-W/H in psychiatric diseases.

Type 2 diabetic mellitus (T2DM) is a disease with high prevalence and a major cause for death worldwide. Diabetic retinopathy (DR) is one of the major manifestation of diabetes. Aldehyde dehydrogenease 2 (ALDH2) detoxifies aldehyde produced during ethanol metabolism and oxidative stress. It has been found that the polymorphism in ALDH2 rs671 is probably associated with the risk of T2DM and DR. However, a lot of inconsistency and controversy still exists. In order to get a more precise and comprehensive estimation for the association between ALDH2 polymorphism with the risk of T2DM and DR, we conducted the present meta-analysis. A comprehensive literature search was conducted using databases, such as Pubmed, Embase, Cochrane Central Register of Controlled Trials, Chinese National Knowledge Infrastructure, and Chinese Biomedical Literature Database, for all related studies. The included studies met the inclusion criteria, such as being case-control studies about the association of ALDH2 polymorphism and T2DM or DR susceptibility, with sufficient data for the present analysis. Eight studies with 2374 cases and 6694 controls were involved in the present meta-analysis. The results indicated a significant lower risk of T2DM for *1/*1 genotype in homozygous models (*1/*1 vs. *2/*2, OR = 0.31, 95% CI = 0.11–0.89, p = 0.03) and in the dominant model (*1/*1 vs. *2/*2 + *1/*2, OR = 0.61, 95% CI = 0.37–1.00, p = 0.05). Subgroup analysis by ethnicity found a significant lower risk of T2DM in Chinese in all genotype models. No significant relation was found between ALDH2 rs671 and DR. In conclusion, the current meta-analysis indicated that ALDH2 rs671 was significantly related with T2DM. The ALDH2 rs671 might be able to be used as a predictor for the risk of T2DM. However, due to the existence of heterogeneity and publication bias in the involved studies, our results should be interpreted with caution.

While upregulation of 2,3-dioxygenase (IDO) accompanied by degradation of tryptophan along the kynurenine pathway have been reported to exert antimicrobial effects against a wide range of infectious agents, its role in the replication of influenza A virus remains uncertain. We performed experiments using influenza A/WSN/33 virus infection of mouse fibroblast cell-line (NIH-3T3) to study the effects of IDO on viral replication. Influenza infection resulted in prominent elevations of transcripts encoding IDO, interferon (IFN)-β, and segment 8 of the virus in NIH-3T3 cells. Introduction of siRNA targeted against IDO followed by infection resulted in further increased levels of viral RNA without altering IFN-β expression. Inhibition of IDO during the infection also resulted in reduction of virus-driven upregulation of 3-hydroxyanthranilate 3,4-dioxygenase (HAAO), but not kynurenine 3-monooxygenase (KMO), which are enzymes downstream in the kynurenine pathway. Thus, induction of IDO appears to contribute to limiting replication of the WSN/33 strain of influenza A virus in murine NIH-3T3 cells.