2020 Vol. 6, No. 4

Cover Story

Hepatitis B is caused by hepatitis B virus (HBV), and persistent HBV infection is a global public health problem, with 257 million people as HBV chronic carriers. Viral covalently closed circular DNA (cccDNA) is a key factor to establish persistent infection in infected hepatocytes. Current antiviral therapies have no direct impact on pre-existing cccDNA reservoir, which can be assembled into minichromosome by hijacking host factors. Understanding the mechanisms of epigenetic regulation in cccDNA minichromosome is crucial to develop new therapy on cccDNA, an attractive target for HBV cure. This review summarizes the current advances in epigenetic regulation of cccDNA minichromosome, which might provide clues to novel druggable targets to cure hepatitis B by either silencing or eliminating cccDNA reservoir.

The emerging role of tubulin posttranslational modifications in cilia and ciliopathies
“At last in” the physiological roles of the tubular ER network
Epigenetic regulation of covalently closed circular DNA minichromosome in hepatitis B virus infection
Long-term high-resolution in vivo imaging of cerebral cortical structures following ischemic stroke
Measurement of viscoelastic properties of injured mouse brain after controlled cortical impact
Prediction of RNA secondary structure with pseudoknots using coupled deep neural networks