This Collection supports and amplifies research related to SDG 3, SDG 5, SDG 10.
Viruses and cancers are deeply intertwined. Globally, one in ten new cancer cases arises in the context of chronic viral infections, with human papillomaviruses (HPVs) and hepatitis B and C viruses (HBV and HCV), each accounting for roughly 5% of new cancers cases worldwide. Other viruses play minor roles — for example, Merkel cell polyomavirus drives rare but aggressive skin cancers.
We would like to invite to this collection contributions that illuminate the multidimensional relationships between viruses and cancers. We welcome studies on well-established oncogenic viruses, emerging links uncovered by large-scale datasets, investigations on the role of microbiota in viral oncogenesis, and mechanistic insights into how viral infections shape the trajectory and evolution of tumors. We also encourage work on the clinical translation of these insights — from diagnostics and screening strategies based on viral and cellular biomarkers to the design of preventive measures and therapeutics.
Through omic and agnostic approaches we are uncovering a broader and more complex picture. We are beginning to uncover possible links between common viral infections and differential cancer risk in ways we did not suspect before. In many instances, the connection is indirect: persistent or chronic infections can reshape or abolish local or systemic immunity, creating an environment where malignant transformation becomes more likely. While such cases may be uncommon, they reveal that cancers may sometimes be an unintended long-term complication of otherwise widespread viral exposures.
It is important to underline that the infectious origin of certain cancers is, in many respects, good news, as we are armed with additional avenues for action against infections. Indeed, we have accumulated centuries of knowledge on how to prevent, diagnose and treat infections, while cancer prevention and therapy remain much more challenging. The successes of HBV vaccination and HPV vaccination illustrate this promise: we are not just preventing infections, but effectively preventing cancer.
This infectious dimension also opens the door to novel diagnostic and preventive strategies. Instead of relying only on the detection of precancerous or cancerous changes, such as the koilocytes sought in the traditional Pap smear (a very specific test), we can now directly detect viral genetic material and detect an infection (a very sensitive test). Molecular tests for HPVs have thus already transformed cervical cancer screening, and similar approaches are expanding into other virus-associated cancers.
At the molecular level, virus-driven cancers display distinctive hallmarks. Viral infections can act in trans on the cellular machinery and contribute to malignant transformation. By modulating cell cycle control, evading immune surveillance, altering signaling pathways, and sustaining chronic inflammation, viruses contribute to the acquisition of cancer hallmarks. While infection alone is rarely sufficient, it accelerates or amplifies the probability that transformed cells will progress toward malignancy.
Oncogenic viruses have not evolved “to cause” cancer, or “because they cause” cancer. Given the very high prevalence of inapparent infections in humans, cancers play a minimal role in the population and evolutionary dynamics of oncogenic viruses. Most oncogenic viruses are part and parcel of the human microbiota. We only start to understand the changes in local and systemic physiology co-occur with changes in the microbiota. Most oncogenic viruses are part and parcel of the common microbiota, and in the vast majority of cases they cause only inapparent and asymptomatic infections. A sound line of evidence suggests that changes in the microbiota, and the associated changes in immune surveillance, may also underlie the transition between an inapparent, asymptomatic infection, and the establishment of a proliferative disease.
The biology of the infected virocell provides unique biochemical, cellular, and tissue context for the processes that underlie cancer. By bringing together diverse perspectives, this collection aims to deepen our understanding of viral oncogenesis and to advance the shared goal of reducing the global burden of cancers.