It's not an easy task to stand on top of a box on London's busy Southbank and try to entertain everyone and anyone in the passing crowds of tourists, school pupils, city workers and arts lovers. Even if you are a stand-up comedian, performance artist, or street entertainer, it would probably still be many people's idea of a tough gig.
Standing on that box and engaging people in the latest scientific research surely makes it even harder. Yet it doesn't appear to phase Dr Ravinder Kanda. Ravinder is a research associate in paleovirology and genomics in the Department of Zoology at Oxford University, and she is one of 12 scientists taking part in Soapbox Science on Friday July 5.
The event, supported by L'Oreal UNESCO For Women In Science Scheme, is now in its third year and gets some of the UK's leading female scientists to talk passionately about their subjects to the general public. Its aim is to help eliminate gender inequality in science by raising the profile, and challenging the public's view, of women and science.
OxSciBlog caught up with Ravinder to learn more about her research and what she'd be talking about to all comers from the top of her soapbox on the South Bank.
You also can read an interview with Ravinder about her research and her career in a blogpost on the Soapbox Science website.
OxSciBlog: What are endogenous retroviruses and why are they so interesting?
Ravinder Kanda: Only 2% of our DNA is used to build our bodies. The rest of it – noncoding DNA – is a mixture of old genes that have lost their function, repetitive strings of DNA whose function is not understood, and other elements. Endogenous retroviruses (ERVs) are a kind of noncoding DNA that make up 8% of our DNA. ERVs are all descended from viruses, very like those that cause disease, like HIV, which managed to insert themselves into our ancestors' DNA in the distant past.
OSB: When and how do we think ERVs got incorporated into our DNA?
RK: The way this particular group of viruses, called retroviruses, infect a cell involves inserting themselves into the DNA of the cell – they become part of our DNA. Once inside the DNA of a cell, new copies of the retrovirus can be produced using the cell's machinery. These new copies can then leave the cell and go on to infect other cells. Occasionally, a retrovirus will infect the germ-line cells – the cells that produce sperm and eggs. In this instance, the virus is now part of the DNA of that sperm or egg cell. When fertilisation occurs, this one cell divides to become two. Both cells now contain a copy of the virus. Two cells go on to make four – all have the viral DNA too. When that fertilised egg develops into an adult, every single cell in that individual's body contains the viral DNA. When this happens this virus is known as an endogenous retrovirus, meaning it is within our DNA. It is inherited by all the offspring of that individual.
There are around 100,000 copies of these ERVs in our genome. By comparing the DNA of other primates and mammals, we can estimate how long ago these ERVs inserted into the DNA of our ancestors. For example, it is estimated that the common ancestor of our closest relative, the chimpanzee, and modern day humans existed approximately 8 million years ago. If a particular ERV is present in the DNA of both humans and chimpanzees, we can say that it must have inserted into the DNA of our ancestor more than 8 million years ago. We can then look at the next closest relative, the gorilla, and see if the ERV is present in their DNA. If it is present in the the gorilla, the common ancestor of humans, chimpanzees and gorillas is thought to have existed around 15 million years ago and so we can say that the ERV inserted into the DNA of our ancestors 15 million years ago. Some of the ERV insertions are ancient, dating back 100 million years.
OSB: How might these 'DNA invaders' be good for us?
RK: In some instances, we have managed to 'borrow' some of the viral genes and use them for our benefit. The most famous example is a gene that is involved in pregnancy, specifically with the formation of the placenta. This gene comes from a virus and is essential for the formation of the placenta. Without it we would not be able to reproduce as we do. In other species, there are instances where having a particular ERV gives you some protection against infection from other related retroviruses. For example, sheep have a particular ERV that can block the receptors of a cell, preventing entry into the cell and therefore infection by other related viruses.
OSB: What can ERVs reveal about the evolution of infections in animals and humans?
RK: Many ERVs in our DNA are ancient, indicating that this invasion has been occurring for millions of years. By comparing those viruses that are present in DNA to viruses that currently infect and cause disease, we can see that some of these viruses are very good at making a leap and infecting different species to those in which they were originally found, something called cross-species transmission. For example, we know that HIV was a virus that originally infected primates. The subgroup of viruses to which HIV belongs – lentiviruses – has recently been discovered in the DNA of other species. These discoveries challenge our understanding of how these viruses might change and evolve.
OSB: What further research is needed to understand more about ERVs?
RK: Lots! We are only just beginning to understand what an influential role viruses may have played in many various aspects of the evolution of a species. One consideration is that some viruses can make the leap to infect other species, such as HIV. A better understanding of cross-species transmission, why or how this occurs, and why some viruses are better at doing this than others, may also help us identify potential 'hotspots' of infection. This could allow us to be better prepared against possible future threats.
For me personally, I am interested in the role that ERVs play with regards to offering immunity against infection from other viruses. The idea of using viruses against themselves is an interesting one. However, we need a better understanding of exactly how this occurs. We still have a long way to go.