Oncogenic herpesvirus KSHV triggers hallmarks of alternative lengthening of telomeres

Timothy P. Lippert, Paulina Marzec, Aurora I. Idilli, Grzegorz Sarek, Aleksandra Vancevska, Mark Bower, Paul J. Farrell, Päivi M. Ojala, Niklas Feldhahn and Simon J. Boulton ()
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Timothy P. Lippert: The Francis Crick Institute
Paulina Marzec: The Francis Crick Institute
Aurora I. Idilli: The Francis Crick Institute
Grzegorz Sarek: The Francis Crick Institute
Aleksandra Vancevska: The Francis Crick Institute
Mark Bower: Department of Oncology, Chelsea & Westminster Hospital
Paul J. Farrell: Imperial College London
Päivi M. Ojala: Imperial College London
Niklas Feldhahn: Centre for Haematology
Simon J. Boulton: The Francis Crick Institute

Nature Communications, 2021, vol. 12, issue 1, 1-11

Abstract: Abstract To achieve replicative immortality, cancer cells must activate telomere maintenance mechanisms to prevent telomere shortening. ~85% of cancers circumvent telomeric attrition by re-expressing telomerase, while the remaining ~15% of cancers induce alternative lengthening of telomeres (ALT), which relies on break-induced replication (BIR) and telomere recombination. Although ALT tumours were first reported over 20 years ago, the mechanism of ALT induction remains unclear and no study to date has described a cell-based model that permits the induction of ALT. Here, we demonstrate that infection with Kaposi’s sarcoma herpesvirus (KSHV) induces sustained acquisition of ALT-like features in previously non-ALT cell lines. KSHV-infected cells acquire hallmarks of ALT activity that are also observed in KSHV-associated tumour biopsies. Down-regulating BIR impairs KSHV latency, suggesting that KSHV co-opts ALT for viral functionality. This study uncovers KSHV infection as a means to study telomere maintenance by ALT and reveals features of ALT in KSHV-associated tumours.

Date: 2021
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DOI: 10.1038/s41467-020-20819-4

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