Since late 2006, honeybees in Europe and North America have been mysteriously disappearing. Once abuzz with activity, hives suddenly turned into honeycombed Marie Celestes. They still had plentiful supplies of honey, pollen and youngsters but the adult workers vanished with no traces of their bodies. The phenomenon has been dubbed colony collapse disorder (CCD). In the first winter when it struck, US hive populations crashed by 23% and in the next winter, they fell again by a further 36%.
Eager to avert the economic catastrophe that a bee-less world, scientists have been trying to find the cause behind the collapse. Amid wackier explanations like mobile phone radiation and GM crops, the leading theories include sensitivity to pesticides, attacks by the vampiric Varroa mite or a parasitic fungus called Nosema, infections by various viruses, or combinations of these threats.
In 2007, US scientists thought they had revealed the main villain in the piece, by showing that the an imported virus – Israeli acute paralysis virus (IAPV)- was strongly linked to empty hives. But since then, another group showed that IAPV arrived in the US many years before the first signs of CCD were reported. Other related viruses have also been linked to CCD hives, including Kashmir bee virus (KBV) and deformed wing virus (DWV).
To pare down these potential culprits, Reed Johnson from the University of Illinois compared the genetic activity of bees from over 120 colonies, including some affected by CCD and healthy ones that were sampled before the vanishing began. He looked at their digestive systems – one of the most places where infections and environmental toxins would start wreaking havoc.
The analysis didn’t offer any simple answers, but Johnson found some evidence to suggest that CCD bees have problems with producing proteins. In animal cells, proteins are manufactured in molecular factories called ribosomes. These factories assemble proteins by translating instructions encoded within molecules of RNA. Ribosomes themselves are partially built form a special type of RNA known as rRNA. And when Johnson looked at the guts of CCD bees, he found unusually high levels of fragmented rRNA.
It’s not entirely clear what causes these fragments, although some of the viruses implicated in CCD have been known to attack and interfere with ribosomes. Nor is it clear what the presence of the rRNA fragments means for the bees. One plausible explanation is that the CCD bees have more broken ribosomes, and have problems with producing proteins on demand. That in turn would limit their ability to respond to environmental threats like pesticide poisoning or viral infections.
On the surface, it looks like Johnson has discovered a tidy chain of events. Multiple viral infections could lead to CCD, via an inability to produce new proteins that renders bees susceptible to pesticides, parasites and other threats. Indeed, although Johnson found that no single infection separated the CCD colonies from the healthy ones, the sick bees were generally carrying a higher burden of viruses and parasites.
But this tale is more complicated than it seems. Other than an abundance of rRNA, Johnson found that 65 genes that were activated differently among sick bees compared to healthy ones. Many of the affected genes have no known function yet. However, none of these were known immune genes, which you would expect to be deployed in response to infections, or detox genes, which would help to nullify any poisons that the bees inadvertently consumed. While these pattern’s aren’t enough to rule out the influences of pesticides or diseases, they certainly don’t support the ideas.
The next step for Johnson is to try and show that being infected with many viruses results in more rRNA fragments, malfunctioning ribosomes, fewer important proteins and poorer health. Until then, the CCD mystery remains open.
Reference: PNAS doi:10.1073/pnas.0906970106
Image: Bee by Bjorn Appel
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