Could viral immunity be the key to cancer treatment?
- Publication Date
- Professor Dorothy H. Crawford
General knowledge about viruses has recently escalated and most people now appreciate how viruses can spread easily, causing epidemics or even pandemics. However, those causing acute infectious diseases are just the tip of the iceberg.
In contrast to acute infections, many viruses silently infect our bodies and reside within us for life. Some are completely harmless, others cause chronic disease, and on rare occasions some of these viruses can turn nasty and induce tumours.
In 1964, the first human tumour-inducing virus was discovered by London-based virologist Anthony Epstein (now Sir Epstein).
The discovery began when Epstein attended a lecture by Denis Burkitt, a British surgeon working in Uganda, where he described the most common childhood tumour diagnosed in his clinic. It usually occurred in the jaw; was rapidly fatal if untreated and was restricted to patients in low-lying areas in central Africa.
Epstein was convinced this tumour was caused by a virus, and after two years’ work on biopsy material sent from Burkitt’s clinic in Africa, he was proved right. By culturing cells from the tumours – later named Burkitt’s lymphoma – and examining them using electron microscopy, he eventually found what he was looking for – a virus. Following his discovery, the virus was then named the ‘Epstein-Barr virus’ (EBV) after Epstein and his late graduate student, Dr Yvonne Barr.
Since those early days, six more human tumour viruses have been uncovered, with these seven now being responsible for around 15% of all human cancers, including common killers such as cervical cancer in women and certain liver and stomach cancers, as well as proportion of Hodgkin’s lymphoma.
The interesting thing about tumour viruses is the number of individuals infected compared with those who later develop tumours. Tumours only occur in a small number of those infected and those which develop often only occur within a restricted geographical area, akin to Burkitt’s lymphoma in central Africa. They are more common in people with suppressed immunity such as transplant recipients. All of these factors suggest other co-factors are required for tumour production.
In the case of African Burkitt’s lymphoma, we know EBV infection is ubiquitous, but the geographical prevalence of tumours largely mirrors year-round, high-frequency malaria infection. As such, it shows that childhood malaria infection induces a lack of immune control of EBV which, along with a genetic change found in the EBV-infected cells, induces tumour outgrowth.
Identifying a virus causing a tumour is not just an academic exercise, since the virus can act as an early target for tumour prevention and therapy. In this regard, experimental immunotherapy has successfully treated EBV-associated tumours in transplant recipients.
There are also early examples of success in vaccination against the papilloma viruses mostly responsible for cervical cancer. Since beginning in the UK in 2008, vaccinations have already produced a dramatic drop in infection rates and potential cancerous tumours among the immunised cohort. As ongoing research hits the clinic, I am confident more good news will follow.
Professor Graeme Ackland is Professor of Computer Simulation at The University of Edinburgh, a researcher at the Higgs Centre for Theoretical Physics, and a Fellow of the Royal Society of Edinburgh.
The RSE’s blog series offers personal views on a variety of issues. These views are not those of the RSE and are intended to offer different perspectives on a range of current issues.