Abstract
Human hepatitis delta virus (HDV) is a small defective RNA satellite virus that requires hepatitis B virus (HBV) envelope proteins to form its own virions. The HDV genome possesses a single coding open reading frame (ORF), located on a replicative intermediate, the antigenome, encoding the small (s) and the large (L) isoforms of the delta antigen (s-HDAg and L-HDAg). The latter is produced following an editing process, changing the amber/stop codon on the s-HDAg-ORF into a tryptophan codon, allowing L-HDAg synthesis by the addition of 19 (or 20) C-terminal amino acids. The two delta proteins play different roles in the viral cell cycle: s-HDAg activates genome replication, while L-HDAg blocks replication and favors virion morphogenesis and propagation. L-HDAg has also been involved in HDV pathogenicity. Understanding the kinetics of viral editing rates in vivo is key to unravel the biology of the virus and understand its spread and natural history. We developed and validated a new assay based on next-generation sequencing and aimed at quantifying HDV RNA editing in plasma. We analyzed plasma samples from 219 patients infected with different HDV genotypes and showed that HDV editing capacity strongly depends on the genotype of the strain.
Highlights
Hepatitis delta virus (HDV) is a small defective RNA virus that infects humans already chronically carrying hepatitis B virus (HBV)
25 nucleotides 30 downstream, called the dsRNA binding motif (DRBM), which defines the minimal editing substrate for acting on double stranded RNA (ADAR)-1. This structure is required for the initiation of editing [20,21], and we recently showed that it can vary according to the HDV genotype [9]
There was no correlation between the initial HDV viral loads and the editing rate values (Table 1), we found a significant correlation between high editing rate levels and low HBV
Summary
Hepatitis delta virus (HDV) is a small defective RNA virus that infects humans already chronically carrying hepatitis B virus (HBV). HDV has been assigned to the Deltavirus genus. New HDV RNA-like sequences have been recently identified in the animal kingdom [2,3,4,5]. Human HDV infection is widespread, and its prevalence differs between areas. Among the 257 million individuals with chronic HBV infection, approximately 15–20 million are infected with HDV. HDV infection is associated with the most severe forms of viral hepatitis, ranging from acute and sometimes fulminant disease to a rapidly progressive form of chronic viral hepatitis rapidly leading to cirrhosis and hepatocellular carcinoma [8]
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