Efficacy of Immune Checkpoint Inhibitors and Oncoviruses in Solid Tumors

A significant proportion of cancers worldwide - estimated at 12% to 20%, is linked to infections, particularly viruses. Among the most important are human papillomavirus (HPV), hepatitis B and C viruses, and Epstein–Barr virus. These infections are common, and in most cases, the body successfully clears them. However, when they persist over time, they can contribute to the development of cancer.

Viruses can promote cancer through several mechanisms. They may interfere with the normal functioning of cells by altering their DNA, disrupting key protective pathways, or promoting chronic inflammation. In some cases, viral proteins directly affect how cells grow and divide, preventing them from repairing damage or undergoing normal cell death. Over many years, these changes can accumulate and eventually lead to the formation of tumors.

In recent years, immunotherapy has emerged as a major breakthrough in cancer treatment. Unlike traditional therapies that directly target tumor cells, immunotherapy works by stimulating the patient’s own immune system to recognize and attack cancer. This approach has shown particularly promising results in certain cancers associated with viral infections, as these tumors often display signals that make them more visible to the immune system.

However, the effectiveness of immunotherapy varies depending on the type of cancer and the individual patient. While some virus-related cancers respond very well, others show more limited or inconsistent benefits. This variability reflects the complexity of both the immune system and the tumor microenvironment, which can either support or hinder the immune response.

Understanding how viruses influence cancer development and how the immune system interacts with these tumors is therefore essential. It not only helps identify which patients are most likely to benefit from immunotherapy but also guides the development of more targeted and personalized treatment strategies.

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