Journal
NATURE GENETICS
Volume 52, Issue 3, Pages 320-+Publisher
NATURE PORTFOLIO
DOI: 10.1038/s41588-019-0558-9
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Funding
- Ontario Institute for Cancer Research (OICR) - government of Ontario
- Leibniz Association [SAW-2015-IPB-2]
- German Center for Infection Research [TTU 01.801]
- German Federal Ministry of Education and Research (BMBF BioTop grant) [01EK1502C]
- German Federal Ministry of Education and Research (ICGC-DE-Mining grant) [01KU1505A-G]
- Cancer Research UK [C5047/A14835/A22530/A17528]
- Dallaglio Foundation
- Bob Champion Cancer Trust
- Masonic Charitable Foundation
- King Family
- Stephen Hargrave Trust
- Swiss National Science Foundation [S-87701-03-01]
- BBSRC [BBS/E/T/000PR9818] Funding Source: UKRI
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Viral pathogen load in cancer genomes is estimated through analysis of sequencing data from 2,656 tumors across 35 cancer types using multiple pathogen-detection pipelines, identifying viruses in 382 genomic and 68 transcriptome datasets. Here, as part of the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, for which whole-genome and-for a subset-whole-transcriptome sequencing data from 2,658 cancers across 38 tumor types was aggregated, we systematically investigated potential viral pathogens using a consensus approach that integrated three independent pipelines. Viruses were detected in 382 genome and 68 transcriptome datasets. We found a high prevalence of known tumor-associated viruses such as Epstein-Barr virus (EBV), hepatitis B virus (HBV) and human papilloma virus (HPV; for example, HPV16 or HPV18). The study revealed significant exclusivity of HPV and driver mutations in head-and-neck cancer and the association of HPV with APOBEC mutational signatures, which suggests that impaired antiviral defense is a driving force in cervical, bladder and head-and-neck carcinoma. For HBV, HPV16, HPV18 and adeno-associated virus-2 (AAV2), viral integration was associated with local variations in genomic copy numbers. Integrations at the TERT promoter were associated with high telomerase expression evidently activating this tumor-driving process. High levels of endogenous retrovirus (ERV1) expression were linked to a worse survival outcome in patients with kidney cancer.
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