Abstract
The hepatitis B virus (HBV) chronically infects over 250 million people worldwide and is one of the leading causes of liver cancer and hepatocellular carcinoma. HBV persistence is due in part to the highly stable HBV minichromosome or HBV covalently closed circular DNA (cccDNA) that resides in the nucleus. As HBV replication requires the help of host transcription factors to replicate, focusing on host protein–HBV genome interactions may reveal insights into new drug targets against cccDNA. The structural details on such complexes, however, remain poorly defined. In this review, the current literature regarding host transcription factors’ interactions with HBV cccDNA is discussed.
Highlights
The hepatitis B virus (HBV) is estimated to chronically infect 257 million people worldwide [1].Chronic HBV infection can promote liver fibrosis and cirrhosis and is independently associated with hepatocellular carcinoma [2,3,4,5,6,7]
The HBV genome is comprised of four overlapping open reading frames (ORFs) that code for formation of closed circular DNA (cccDNA) and control cccDNA copy numbers remain elusive
TATA box protein (TBP) is a ubiquitous transcription factor that is crucial for host transcription initiation and is functional once bound to the transcription factor IID (TFIID) complex [176]
Summary
The hepatitis B virus (HBV) is estimated to chronically infect 257 million people worldwide [1]. A feature common to all viruses, including HBV, is the requirement of their genome to interact with host proteins to complete the viral replication cycle. Targeting this interaction between the HBV cccDNA and host proteins could represent a potential therapeutic target. Transcription factors function by interacting with DNA sequences upstream of the gene to be transcribed, i.e., promoter regions, to control transcriptional activity, where regulation can take the Viruses 2020, 12, 160; doi:10.3390/v12020160 www.mdpi.com/journal/viruses. Transcription factors function by interacting with DNA sequences upstream of the gene to be transcribed, i.e., promoter regions, to control transcriptional activity, where regulation can take the form of of initiation initiationand/or and/orinhibition inhibition transcription [11,12].
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