Can a trigger-happy immune system cause cancer after viral infection?

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HPV cellsSource: The Guardian – Cath Ennis.

Friendly fire: while the immune system tries to protect us from viruses, it could be causing cancer.

The immune system is a fickle thing, both hero and villain.

The ability of our ancestors to survive plague and pestilence was one of the forces that shaped the evolution of the human species into its current form. But many of us now find ourselves in environments where many of the biggest infectious threats have been neutralised by a combination of vaccination programmes, improved hygiene, and (temporarily) effective treatments. With their usual duties cut back so drastically, our evolutionary superstar immune systems sometimes lash out at innocuous perceived threats. This can cause allergies, multiple sclerosis, and other auto-immune disorders in the process – sins of commission, if you will.

But at least our immune systems are still pretty good at protecting us from infections and most cancers, right?

Well, much of the time, yes. The importance of the immune system in protecting us from cancer is evident from the increased rates of the disease in people with reduced immunity due to HIV/Aids or following organ transplants. And yet the immune system’s sins of omission mean that far too many cancer cells slip through the net – and we still get colds and the dreaded norovirus, too.

This week, though, new research from University College London (UCL) suggests for the first time that the immune system also commits sins of commission when it comes to cancer.

The research, published in the journal Cell Reports, concerns a class of genes called the APOBEC family. These genes code for proteins that attack invading viruses by mutating their DNA, a tactic that can stop or at least slow the replication and spread of the virus. The mutations caused by APOBEC proteins occur in a characteristic pattern – a pattern that also shows up in some types of cancer, including types that are often caused by infection with human papilloma viruses (HPV). Could the mutations in these cancers be caused by misfiring antiviral defences?

Drs Stephen Henderson, Tim Fenton and their teams at UCL have now demonstrated that there is indeed an association between the presence of HPV in some cancer cells, elevated activity of the APOBEC proteins in those cells, and the presence of the characteristic APOBEC-mediated mutation pattern. These findings support the idea that HPV infection triggers an anti-viral attack that not only hits the intended target – the viral genes –but also the cell’s own DNA. The UCL team also found that mutations caused by APOBEC have a strong tendency to hit genes such as PIK3CA that help to regulate the growth and division of the cell, and whose mutation is associated with the development of cancer…read the full story.

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The ONA Editor curates oncology news, views and reviews from Australia and around the world for our readers. In aggregated content, original sources will be acknowledged in the article footer.

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