Decoding Cancer Mutational Signatures in Host and Viral Genomes

ABSTRACT

Epstein–Barr virus (EBV) is linked to several human cancers, including nasopharyngeal carcinoma, gastric cancer, and some lymphomas. In these tumours, the host cancer genome accumulates characteristic mutational signatures that reflect the activity of specific DNA damage and repair processes. However, it remains unclear whether the EBV genome itself carries the same mutational footprints as the host genome. This project will investigate whether mutational signatures identified in EBV-associated cancer cells are mirrored in the viral genome, providing insight into how mutational processes operate across both host and pathogen DNA.

Using whole-genome sequencing data from EBV-positive cancers, we will compare mutational patterns in the human cancer genome with those in the associated EBV genomes. We will test whether the same signatures are present in both compartments and whether shared patterns point to common molecular mechanisms, such as replication stress or dysregulated replication machinery. By integrating bioinformatics analyses of somatic mutations and viral sequence variation, this project aims to uncover whether host- and virus-derived mutations arise from overlapping biological processes or from distinct mechanisms shaped by the tumour environment.

Research Questions:

Do EBV genomes in EBV-associated cancers exhibit mutational signatures similar to those found in the host cancer genome?
Can similarities between host and viral mutational signatures reveal underlying mechanisms related to DNA replication or repair machinery?

SKILLS & EXPERIENCE REQUIRED

Bioinformatics, coding, biomedical sciences