Getting Rid of a Persistent Troublemaker to Cure Hepatitis

See allHide authors and affiliations

Science  14 Mar 2014:
Vol. 343, Issue 6176, pp. 1212-1213
DOI: 10.1126/science.1252186

You are currently viewing the summary.

View Full Text

Log in to view the full text

Log in through your institution

Log in through your institution


One of the major enigmas in hepatitis B virus (HBV) infection is the striking persistence of its episomal DNA [covalently closed circular DNA (cccDNA)], the viral transcriptional template sequestered in the nucleus of infected hepatocytes. Eradicating cccDNA is a requisite for virus elimination and cure, a desirable end point for the 400 million people chronically infected by HBV worldwide who are at a substantial risk for end-stage liver disease and liver cancer. Commonly used therapies suppress viral replication, but because they are ineffective at targeting the cccDNA pool, they often require lifelong administration to prevent viral rebound (1). Thus, the development of new drugs that efficiently and specifically target HBV cccDNA is a priority. On page 1221 of this issue, Lucifora et al. (2) uncover a mechanism that destroys cccDNA, which can be activated by two different approaches.