It’s finally out. After months of will-they-won’t they and should-they-shouldn’t-they deliberations, Nature has finally published a paper about a mutant strain of bird flu that can spread between mammals.
The strain was produced by Yoshihiro Kawaoka from the University of Wisconsin-Madison, who was trying to understand whether wild bird flu viruses have the potential to start a pandemic. These viruses can occasionally infect humans, but so far, they’ve been contained by their inability to efficiently jump from human to human. Kawaoka’s work makes it clear that they can evolve that ability.
Kawaoka’s study, along with a similar one from Ron Fouchier, has been the subject of intense debate for the last several months (catch up on the backstory here). What are the benefits of the research, and do they outweigh the risks? Now that the paper is finally out, we can start to answer those questions.
I’ve written about the paper for Nature News, focusing very heavily on the science rather than the politics. Head over there for a tighter version of this story. In this post, I’m going to highlight four important themes from the paper.
Around 8 to 10 per cent of your DNA comes from viral ancestors. These sequences are the remains of prehistoric viruses that inserted their DNA into the genes of our ancestors, hundreds of millions of years ago. Some of them became permanent residents, and were passed down from parent to child. These endogenous retroviruses, or ERVs, are a legacy of epidemics past.
We understand how ERVs got into our DNA in the first place. But why have they been such successful invaders, to the point where they fill around a tenth of our genome? Gkikas Magiorkinis from the University of Oxford has an answer. By comparing the ERVs of 38 mammals, from humans to dolphins, he has found that the critical step in these invasions was the moment when the viruses hung up their coats.
In a French meadow, a creature that specialises in corrupting the bodies of other animals is getting a taste of its own medicine.
Leptopilina boulardi is a wasp that lays its eggs in fly maggots. When the wasp grub hatches, it devours its host form the inside out, eventually bursting out of its dead husk. A maggot can only support a single grub, and if two eggs end up in the same host, the grubs will compete with one another until only one survives. As such, the wasps ensure that they implant each target with just one egg. And if they find a maggot that has already been parasitized by another L.boulardi, they usually stay away.
Usually, but not always.
L.boulardi is sometimes infected by a virus called LbFV, which stands for L.boulardi filamentous virus. And just as the wasp takes over the body of its maggot target, so the virus commandeers the body of the wasp. It changes her behaviour so that she no longer cares if a maggot is already occupied. She will implant her eggs, even if her target has an existing tenant. After infected wasps are finished, a poor maggot might have up to eleven eggs inside it.
Yesterday, I attended a conference at the Royal Society to discuss the controversial studies on mutant H5N1 flu viruses that can spread between mammals. It was the first time that the two scientists behind the papers – Yoshi Kawaoka and Ron Fouchier – have appeared in public together since the controversy broke, and Kawaoka spoke openly about his results.
Late last year, two teams of scientists announced that they had mutated the H5N1 ‘bird flu’ virus so that it can spread easily between mammals, an ability that their wild cousins lack. The research aimed to understand how natural viruses could evolve into more dangerous forms. But it also raised concerns that the mutant strains could cause a pandemic if they were accidentally released or used in a terrorist attack. (For the background to this controversy, here’s my explainer.)
Last year, the US National Science Advisory Board for Biosecurity (NSABB) – an independent advisory board to the government – recommended that both papers should be published with significant redactions. The full information would only be released to selected scientists. But on 30 March, after a two-day meeting, the NSABB announced that it had changed its mind.
The scientists who led the research – Ron Fouchier from Erasmus Medical Center in Rotterdam, and Yoshihiro Kawaoka from University of Wisconsin-Madison – have since revised their papers. The NSABB voted unanimously to publish Kawaoka’s altered manuscript. Fouchier’s was more contentious, but the board voted 12 to 6 in favour of publishing it.
These recommendations are not the final word. Both manuscripts still have to go through the usual process of peer review, and the US government hasn’t weighed in yet. But should the process now go smoothly, nothing will be redacted from either paper. Fouchier has confirmed that his manuscript will include the full genetic sequence of his mutant strain.
What prompted this U-turn? Fouchier and Paul Keim, acting chair of the NSABB, spoke about the decision at a press conference this morning, held ahead of a Royal Society meeting on Tuesday and Wednesday.
For a few months now, an intense debate has raged around two mutant strains of H5N1 ‘bird’ flu that, unlike their wild counterparts, can spread easily between mammals. The strains, created by two teams of scientists, have prompted fears that they might be trigger a pandemic, after being accidentally released or used in bio-terrorism. To counter those objections, proponents of the research have argued that we need to study how flu viruses spread and mutate, so that we can better prepare for the very real risk of a natural pandemic.
It’s a tricky issue. Over at Nature News, I’ve written an explainer that lays out what the viruses are, what the two teams have done to them, and some of the risks and benefits of the research. Head over there to get some basics about the story. I’d also highly recommend Carl Zimmer’s new piece for the NYT, which covers one of the risks that I didn’t.
It is dawn in a European forest, and gypsy moth caterpillars are looking for somewhere to hide. With early birds starting to rise, the caterpillars will spend the day in bark crevices or buried in soil. But one of them is behaving very strangely. While its peers head downwards, this one climbs upwards, to the very top of the highest leaves. It has come to die.
At the top of its plant, the caterpillar liquefies. Its body almost seems to melt. As it does, it releases millions of viruses, dripping them onto plants below and releasing them into the air. These viruses are the agents that compelled the caterpillar to climb, and eventually killed it. They are baculoviruses, and they cause a condition known aptly as Wipfelkrankheit – the German for “tree top disease”.
“The discovery of HIV enables us to develop a vaccine to prevent AIDS in the future… We hope to have such a vaccine ready for testing in approximately two years.” – Margaret Heckler, Secretary of Health and Human Services, April 23, 1984.
Twenty-seven years have passed since Heckler’s comment and no vaccine exists. There is a simple reason for this: HIV out-evolves us. HIV can produce around 100 billion new virus particles every day, and it does so with unusual imprecision. When most genetic material is copied with great fidelity, HIV goes for a sloppier approach. It duplicates itself with errors galore, creating a swarm of genetically variable viruses. It leaves a host looking very different to when it entered.
In the face of this rapid shape-shifting, any drug or vaccine soon becomes obsolete. Fighting HIV is like fighting a hydra – there are several heads and every time you lop one off, two more grow in its place.
Every year, in mid-September, big brown bats throughout Colorado head for their favourite roosts, where they will spent the winter in hibernation. But some of the bats won’t sleep alone – they are carrying the rabies virus, and it will also hibernate through the winter in its slumbering host.
The rabies virus is a killer. Infections are almost always fatal, and around 55,000 people around the world succumb to the virus every year. Dogs are the leading carriers, but in North America, vaccination programmes have effectively eliminated dog rabies. Bats are another story – they are far more difficult to vaccinate and they have overtaken man’s best friend as the leading cause of American rabies.
Now, Dylan B. George from Colorado State University has shown that the rabies virus, by hibernating alongside the big brown bats, gets a free pass to the next generation.
You have a sculpture, an intricate piece of modern art, covered in bulges and blisters. Your task is to weave a cover for it. The fit must be exact. You have to fill in every dent and wrap around every lump. Here’s the catch: you have to make this faultless shroud from a single piece of string that must automatically weave itself into the right three-dimensional shape.
This is the challenge that Sarel Fleishman, Timothy Whitehead and Damian Ekiert from the University of Washington have just overcome. Their “sculpture” is a protein called haemagglutinin, or HA, which sits on the surface of flu viruses. Their “shroud” is another protein designed to perfectly fit onto the contours of HA and neutralise it. They have found a way of fashioning these designer proteins on a computer – a feat that could make it easier to create the next generation of anti-flu drugs.