A simplified qPCR method revealing tRNAome remodeling upon infection by genotype 3 hepatitis E virus

The landscape of tRNA–viral codons regulates viral adaption at the translational level, presumably through adapting to host codon usage or modulating the host tRNAome. We found that the major zoonotic genotype of hepatitis E virus (HEV) has not adapted to host codon usage, prompting exploration of the effects of HEV infection on the host tRNAome. However, tRNAome quantification is largely impeded by the extremely short sequences of tRNAs and redundancy of tRNA genes. Here, we present a length-extension and stepwise simplified qPCR method that utilizes a universal DNA/RNA hybrid tRNA adaptor and degenerate primers. Using this novel methodology, we observe that HEV infection dramatically reprograms the hepatic tRNAome, which is likely to facilitate translation of viral RNAs. This tRNAome quantification method bears broad implications for future tRNA research and possibly tRNA-based diagnostics

Comparison of TiO2 and g-C3N4 2D/2D nanocomposites from three synthesis protocols for visible-light induced hydrogen evolution

Knowledge of the interfacial structure of nanocomposite materials is a prerequisite for rational design of nanostructured photocatalysts. Herein, TiO2 and g-C3N4 2D/2D nanocomposites were fabricated from three distinct synthetic protocols (i.e., co-calcination, solvothermal treatment and charge-induced aggregation), showing different degrees of enhancement (1.4-6.1 fold) in the visible-light induced photocatalytic hydrogen evolution reaction compared to the simple physical mixture. We propose that the interfacial TiO- N covalent bonding promotes the charge carrier transfer and separation more effectively than the electrostatic interaction, thus accelerating the photocatalytic H-2 production. Meanwhile, the exposed surface area of TiO2 in the composite needs to be enlarged for deposition of the co-catalyst. This research sheds light on the rational design of hybrid nanocomposites based on earth-abundant elements for photocatalysis

The macrolide antibiotic azithromycin potently inhibits hepatitis E virus in cell culture models

Hepatitis E virus (HEV) infection in immunocompromised patients, pregnant women and children requires treatment; however, no approved medication is currently available. The macrolide antibiotic azithromycin has been identified as a potent HEV inhibitor. Azithromycin inhibits HEV replication and viral protein expression in multiple cell culture models with genotype 1 and 3 strains. This is largely independent of its induction of an interferon-like response. Because it is safe and cheap, repurposing azithromycin for treating HEV infection is attractive, particularly in resource-limited settings.</p

Ivermectin effectively inhibits hepatitis E virus replication, requiring the host nuclear transport protein importin α1

We show that ivermectin, an FDA-approved anti-parasitic drug, effectively inhibits infection with hepatitis E virus (HEV) genotypes 1 and 3 in a range of cell culture models, including hepatic and extrahepatic cells. Long-term treatment showed no clear evidence of the development of drug resistance. Gene silencing of importin-α1, a cellular target of ivermectin and a key member of the host nuclear transport complex, inhibited viral replication and largely abolished the anti-HEV effect of ivermectin.</p