What is it about?
This study shows that EBV and KSHV hijack the host kinase NEK2 through viral latency proteins to drive chromosomal instability and tumor growth. Targeting NEK2 impairs survival of virus-infected cancer cells, highlighting a potential therapeutic strategy.
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Why is it important?
Some viruses can trigger cancer, but treatment options remain limited. In this study we found that EBV and KSHV hijack a human protein kinase called NEK2 to drive tumor growth. Blocking NEK2 weakens virus-driven cancer cells, suggesting a new and potentially more targeted treatment approach.
Perspectives
This represents an exciting intersection of virology and cancer biology. It highlights how oncogenic viruses do not simply introduce viral oncogenes but actively rewire host cellular machinery to sustain malignant growth. Discovering that EBV and KSHV converge on a common host kinase, NEK2, was particularly striking because it reveals a shared vulnerability in virus-driven cancers. We are especially encouraged by the translational potential of these findings—that targeting a host factor like NEK2 may provide a new therapeutic strategy for malignancies that currently lack effective, virus-specific treatments. Beyond its immediate implications, this work reinforces the broader concept that understanding virus–host interactions can uncover fundamental mechanisms of tumor biology and reveal new opportunities for precision therapy.
Erle Robertson
University of Pennsylvania
Read the Original
This page is a summary of: Human oncogenic herpesvirus latency proteins activate NEK2 to promote chromosomal instability and tumorigenesis, Proceedings of the National Academy of Sciences, February 2026, Proceedings of the National Academy of Sciences,
DOI: 10.1073/pnas.2535073123.
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