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Amplification, Next-generation Sequencing, and Genomic DNA Mapping of Retroviral Integration Sites

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Published on: March 22, 2016

Resolving complex structures at oncovirus integration loci with conjugate graph.

Wenlong Jia¹, Chang Xu¹, Shuai Cheng Li¹

¹Department of Computer Science, City University of Hong Kong, Hong Kong.

Briefings in Bioinformatics

|August 31, 2021

Summary

This summary is machine-generated.

This study introduces a new graph model to map viral DNA integrations in cancer genomes. The findings reveal distinct patterns of viral integration for human papillomavirus (HPV) and hepatitis B virus (HBV), offering insights into cancer development.

Keywords:

cancer genomics complex structure conjugate graph structural variation virus integration

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Identification of Functionally-Relevant Lentivirus Integration Sites in an Insertional Mutagenesis Cell Library

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Published on: January 10, 2025

Area of Science:

Genomics
Virology
Bioinformatics

Background:

Oncovirus integrations lead to genomic alterations like copy number and structural variations (SVs).
The impact of integrated viral DNA on host genome function is not fully understood.
Reconstructing the local genomic map (LGM) of integrated oncoviruses is crucial for understanding their emergence and effects.

Purpose of the Study:

To develop a computational method for reconstructing rearranged LGMs at oncovirus integration sites.
To investigate the biological insights of oncovirus integrations in HPV and HBV-infected cancers.
To identify patterns and mechanisms of viral DNA integration in host genomes.

Main Methods:

Proposed a conjugate graph model to reconstruct the rearranged LGM at integrated loci.
Validated the algorithm using simulation tests.
Applied the algorithm to whole-genome sequencing data from HPV and HBV-infected cancer samples.

Main Results:

Observed four distinct patterns of oncovirus integration: coding-frame truncation, tumor gene hyper-amplification, and viral cis-regulation in introns or intergenic regions.
Identified frequent focal duplicates and host SVs in HPV-integrated LGMs, contrasting with prevalent focal deletions in HBV-integrated LGMs.
Found evidence suggesting enhanced microhomology-mediated end joining in both HPV and HBV integrations, with HPV integrations potentially occurring during DNA replication.

Conclusions:

The developed conjugate graph model reliably reconstructs viral-integrated LGMs, providing foundational understanding of oncovirus integration.
Distinct integration patterns and mechanisms were identified for HPV and HBV, offering insights into their oncogenic roles.
The study highlights the potential role of DNA replication and microhomology-mediated end joining in viral integration processes.