Tracking the history of hepatitis C to help tackle epidemics
Gkikas Magiorkinis, a clinical research fellow from the Department of Zoology at Oxford University in the United Kingdom, has traced history at a microscopic level. By combining epidemiological and molecular data, he has shown how hepatitis C spreads in a population, underlining early diagnosis as a key to preventing the spread of epidemics.
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Symptoms can take up to 20 years to emerge and in that time the disease can spread to other parts of the body. This means that unlike other diseases, such as the flu, where symptoms are apparent within days, it is difficult for people to know where a hepatitis C infection originates. Through his research, Magiorkinis discovered that the most prevalent types of hepatitis C spread worldwide soon after the Second World War, coinciding with the expansion of blood transfusions and intravenous drug use.
His research is a part of the European Union (EU)-funded C THE LIGER project, which comes from the Marie Curie programme of support for research fellows. During that time, Magiorkinis studied molecular evolution and focused his research on endogenous retroviruses (ERVs); normal components of the human genome that are thought to be remnants of ancient germ line infections. In the C THE LIGER project, he developed computer routines and experimental protocols to study ERVs more efficiently.
“ERVs are relics of ancient infections in animal genomes from retroviruses - like the one causing AIDS in humans,” Magiorkinis says. “Like palaeontologists digging under the dirt to find relics of ancient dead animals, in paleovirology we make programmes that ‘mine’ the genomes of animals to find ‘viral fossils’, viruses that used to infect our ancestors millions of years ago. These then got trapped within the genomes of their germ lines (eggs or sperm) and passed through the inheritance into present day animals. Some 8% of our genomes are viruses that got trapped in our ancestors up to 100 million years ago.”
Magiorkinis sees striking similarities between the way ERVs colonise genomes and how viruses spread within a population. He studied four hepatitis C epidemics in Greece, using data from 943 patients collected between 1995 and 2000. He then found that injection drug users were ‘super-spreaders’, each transmitting the virus to 20 other people – and, crucially, that most of the transmissions occurred in the first couple of years. In 2012 he showed that, similarly to epidemic super-spreaders, there are genomic super-spreaders. That is, there are ERVs that can spread within the genomes much more efficiently by changing their life cycles.
Magiorkinis, who won the European Commission's inaugural Marie Curie Prize for Promising Research Talent in 2012, says his model helps build a solid argument to improve early diagnosis and antiviral treatment in high-risk groups. He believes this could be useful for other populations and in other infections, such as HIV.
Hepatitis C is currently thought to infect 180 million people worldwide and most are unaware that they have the disease. About 20% of people infected with hepatitis C can develop cancer or liver scarring, at which point the only treatment is a liver transplant costing over €100,000. As of now, there is no vaccine for the disease.
C THE LIGER’s mentor Robert Belshaw, a lecturer in Genomics at Plymouth University in the United Kingdom, says the research into ERVs could contribute towards the health of the population in Europe. “These are viruses that millions of years ago infected sperm or egg cells and so became embedded into our genomes. Magiorkinis and I wanted to know how they proliferate within us and what effect they have on us,” Belshaw explains.
Belshaw says the Marie Curie fellowship gave Magiorkinis new bioinformatic tools to work in this field, complementing his existing expertise in viral epidemiology. “Because these viruses are also genomic parasites, we need to approach them from a genomic as well as a more traditional, epidemiological angle,” Belshaw says.