A plague on both your mouses

Bioterrorism is making headlines again, drawing attention to ongoing efforts to develop vaccines against potential warfare agents. A group led by Henry Daniell (University of Central Florida, Orlando) has produced an oral vaccine that protects mice from Yersinia pestis, the bacterium that causes pneumonic, septicemic and bubonic plague. Though these diseases can currently be treated with antibiotics, drug-resistant strains of the bacterium have begun to emerge.

The researchers produced the vaccine from tobacco plant chloroplasts, which they genetically engineered to carry an antigen that produces immunity against Y. pestis (Infect. Immun. 78, 3640–3650; 2008). Mice that ingested the vaccine showed no trace of infection despite exposure to lethal doses of the bacterium, whereas all control mice died within 8 d of challenge. Oral administration was substantially more effective than subcutaneous injection.

Injectable Y. pestis vaccines exist, but they are expensive to produce and impractical to store and are therefore no longer commercially available. In an emergency, it would be difficult to generate sufficient quantities of these vaccines and immunize large populations; furthermore, compliance rates for such injections are often quite low. If effective in humans, an oral vaccine for the plague could be a practical means of preventing an epidemic.

Etiology of a parrot disease

Avian proventricular dilatation disease (PDD) was first reported more than 30 years ago, but its cause has remained unknown until recently. An international group of scientists led by Amy L. Kistler (University of California, San Francisco) and Ady Gancz (The Exotic Clinic, Israel) has identified a new bornavirus (avian bornavirus, ABV) in affected parrots that may underlie the disease.

PDD is an inflammatory disease that affects the autonomic nerves of the digestive tract in birds, causing gastrointestinal dysfunction and wasting. It can also affect the central nervous system and have neurologic symptoms. The disease is often fatal. It has been reported in both wild and domesticated psittacine birds, including 50 species of parrots and members of five other orders of birds, such as the endangered Spix's macaw.

Kistler and Gancz analyzed a group of parrots from the US and one group from Israel using microarrays. They found the new ABV sequence in 62.5% of the samples from birds with PDD but not in control samples (J. Virol. doi: 10.1186/1743-422X-5-88; published online 31 July 2008). In a separate group of birds, ABV was present in 71% of those with PDD but not in controls. The researchers conclude that ABV is a leading candidate as the causative agent in PDD, though formal confirmation is needed.

Fruit flies are dopey when sleepy

It's official: too little sleep makes you stupid. Studies have shown that sleep-deprived animals have trouble acquiring new skills and carrying out certain tasks, but until now it was unclear whether learning was truly impaired, or whether subjects' desire to sleep or lack of motivation influenced the results. A rigorous new study in fruit flies strengthens the argument that extended wakefulness is indeed the main source of such learning difficulties (Curr. Biol. 18, 1110–1117; 2008). The researchers show that the damage can be reversed by increasing dopamine expression in a brain structure called the mushroom bodies.

Paul Shaw and colleagues (Washington University School of Medicine, St. Louis, MO) deprived flies of sleep and evaluated their ability to learn to overcome their attraction to light and enter a dark chamber. The longer flies were made to stay awake, the worse they performed on the test. The authors carried out numerous control studies to rule out potential confounding variables.

The researchers determined that the dopamine D1-like receptor was directly involved in the learning deficiency. By activating this receptor in the mushroom bodies only, they managed to repair the learning problems. These findings suggest that dopamine-stimulating drugs may improve learning capabilities in sleep-deprived humans.