Notice: Users may be experiencing issues with displaying some pages on stanfordhealthcare.org. We are working closely with our technical teams to resolve the issue as quickly as possible. Thank you for your patience.
 

COVID-19 Resources »      Vaccine Update »      Visitor Policy »

A classification model for G-to-A hypermutation in hepatitis B virus ultra-deep pyrosequencing reads BIOINFORMATICS Reuman, E. C., Margeridon-Thermet, S., Caudill, H. B., Liu, T., Borroto-Esoda, K., Svarovskaia, E. S., Holmes, S. P., Shafer, R. W. 2010; 26 (23): 2929-2932

Abstract

G ? A hypermutation is an innate antiviral defense mechanism, mediated by host enzymes, which leads to the mutational impairment of viruses. Sensitive and specific identification of host-mediated G ? A hypermutation is a novel sequence analysis challenge, particularly for viral deep sequencing studies. For example, two of the most common hepatitis B virus (HBV) reverse transcriptase (RT) drug-resistance mutations, A181T and M204I, arise from G ? A changes and are routinely detected as low-abundance variants in nearly all HBV deep sequencing samples.We developed a classification model using measures of G ? A excess and predicted indicators of lethal mutation and applied this model to 325 920 unique deep sequencing reads from plasma virus samples from 45 drug treatment-naïve HBV-infected individuals. The 2.9% of sequence reads that were classified as hypermutated by our model included most of the reads with A181T and/or M204I, indicating the usefulness of this model for distinguishing viral adaptive changes from host-mediated viral editing.Source code and sequence data are available at http://hivdb.stanford.edu/pages/resources.html.ereuman@stanfordalumni.orgSupplementary data are available at Bioinformatics online.

View details for DOI 10.1093/bioinformatics/btq570

View details for Web of Science ID 000284430900001

View details for PubMedID 20937597

View details for PubMedCentralID PMC2982158