Group: Group I (dsDNA)
Species: Human adenovirus D (HAdV-D)
Serotype: Human adenovirus 36 (HAdV-36)
AD-36 is one of 51 types of adenoviruses known to infect humans. It has recently been focus of intense research, particularly by Dr. Nikhil Dhurandhar, due to surprising impact on obesity. There has been a positive correlation between the body fat and the presence of AD-36 antibodies in the blood. Previous research showed that chicken or monkeys injected with similar types of viruses show a rapid weight gain.
Could fat be catching?
by Jenny Bryan
Could a fat virus be responsible for the epidemic of obesity that is sweeping the USA and seems to be spreading to Britain? Obesity scientist, Dr Nikhil Dhurandhar thinks that it is and has some intriguing research findings to back him up. But he knows that other obesity specialists cannot believe it’s that simple.
‘The concept of a virus causing obesity is so far away from mainstream causes of obesity that it’s going to take much more convincing and evidence simply because it’s a very different idea. But we’ll do it,’ predicts Dr Dhurandhar, Wayne State University, Detroit, Michigan.
In the USA 61% of people are now officially classed as obese (with a body mass index, BMI, of over 30) or overweight (BMI of 25-30). The situation is scarcely any better in the UK, with about 20% of people obese and over 40% overweight.
If you look at a map of obesity in the USA, you can watch the epidemic spreading rather like a forest fire from the east coast to the west over the last 20 years. And it is this, says Dhurandhar, which suggests that there could be an infection.
It started with chickens …
Dhurandhar’s story starts in Bombay in the 1980s with a mysterious epidemic that wiped out hundreds of thousands of chickens. The birds were found to be infected with an adenovirus called SMAM-1. Adenoviruses are very common. There are at least 40 types that affect humans and they cause about 1 in 20 cases of chest infection.
What was intriguing about the Indian chickens with SMAM-1 was not so much that they were probably killed by an adenovirus infection, but that they died plump, with a large pale liver and large kidneys. They weren’t thin and emaciated as you might expect an animal with a virus to be.
Working in India, Dhurandhar deliberately infected some more chickens with the same virus and, sure enough, these birds also put on weight. He decided to pursue his research in the USA, but the US government wasn’t keen on him importing a virus that had wiped out a large portion of the Indian chicken population.
Instead, Dhurandhar borrowed a human adenovirus, called Ad-36, from the US collection and set to work infecting first chickens and then rhesus monkeys and marmosets. Like the chickens, infected animals started to put on weight. Six months after they were infected, three male marmosets put on three times as much weight and doubled their body fat compared to three animals that were not infected. It was a very small study, but the results were still impressive.
It wouldn’t be ethical to infect humans with Ad-36 to see if they got fat. But, as the virus does occur naturally in the human population, Dhurandhar decided to compare infection rates in people who were fat with those who weren’t. He tested 500 people in three cities. Thirty per cent of obese people screened positive for the Ad-36 virus, compared with only 5 to 10% of those who were not overweight.
How the fat virus might work
Dhurandhar – and his critics – wanted to know how a fat virus might work. Dhurandhar showed that Ad-36 appeared to increase the size and number of fat cells in infected animals. In the laboratory, his experiments suggested that Ad-36 encourages pre-fat cells with the potential to become fat cells to do just that. Three times as many pre-fat cells became fat cells when they were exposed to Ad-36 compared with fat cells that weren’t exposed to the virus.
As part of his studies to try and convince other obesity researchers about the importance of the fat virus, Dhurandhar turned to a set of identical twins, Christyn and Beth. Born with exactly the same genes, there was no chance that one twin was genetically more likely to put on weight than the other. Until they went to college, the twins did indeed remain a very similar weight – as do nearly all sets of identical twins. But in the two years after Christyn left home to go to college, she became two and a half stone heavier than her twin. Blood tests showed that, while Beth remained Ad-36 negative, Christen had, at some point, been infected with the virus. Did the virus make her put on weight or did she just eat more and exercise less when she went to college? Who knows, but Dhurandhar blames it on the virus.
Others remain sceptical.
‘The idea that a virus may be causing obesity seems intrinsically unlikely,’ says Professor Stephen Bloom, from Imperial College, London. ‘Obesity has been growing at a constant rate for about 50 years and the causes are pretty obvious. People have been eating much more and taking less exercise. Why do you need to invent some strange story about a virus?’
Virologist, Professor William Russell, from the University of St Andrews, points out that adenoviruses have never been linked with a long-term illness, like obesity. They cause short-term infections and disappear. It’s important to keep an open mind but, at present, the evidence just does not stack up, he says.
A vaccine against obesity?
In the USA, some scientists are more prepared to accept that viruses could be involved.
‘Viruses can lie dormant for many years and we’ve seen the crossover of the HIV virus, for example, from animals to humans. We may be seeing a similar thing now with the obesity virus,’ suggests Dr John Foreyt from Baylor College, Texas.
‘We really don’t know why people get fat or why people are skinny. There’s so much that is unknown and that’s why we need new theories and people looking at why our bodies are the way they are,’ he says.
One possible hypothesis is that, in the late ’70s, someone working on a chicken farm in India had the Ad-36 virus and came in contact with birds with SMAM-1. The two viruses got together, exchanged genetic material, and turned into a hybrid virus capable of infecting humans and making them fat. There is nothing, of course, to confirm this series of events, but Dr Dhurandhar now has research grants to help him develop his theories. He has his sights set on a vaccine against the fat virus, but accepts that could be some way off:
‘It would be absolutely fascinating to have a vaccine to prevent at least some types of obesity virus – that’s my dream,’ he says.
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