In 2003 and 2004, bird flu outbreaks devastated the economies of several Southeast Asian countries. More than 140 million birds either succumbed to the virus or were culled by humans in an attempt to control the epidemic. Poultry producers lost more than $10 billion.

Thankfully, those strains of avian flu weren’t adept at infecting humans. If a future strain manages to do so in a big way, the resulting pandemic could cost the global economy $1.25 trillion.

Those predictions have ruffled feathers among politicians and scientists alike, and a serious effort has begun to prevent such an occurrence. Unfortunately, research on anti-viral drugs and vaccines is going nowhere fast.

Now however, scientists at the Universities of Cambridge and Edinburgh have chosen to attack the problem in a different way: they’ve created a better chicken.

In a paper published in Science, Laurence Tiley and colleagues report having genetically re-engineered the standard chicken into a version that doesn’t transmit avian flu to its coop-mates. The scientists assert their super-chicken may prevent outbreaks of avian flu among birds and yes, reduce the chances that the virus could jump to humans, who have no immunity to bird flu.

“Preventing virus transmission in chickens should reduce the economic impact of the disease and reduce the risk posed to people exposed to the infected birds,” Tiley said in an interview. “The genetic modification we describe is a significant first step along the path to developing chickens that are completely resistant to avian flu.”

To produce their super-chickens, Tiley’s group introduced a so-called RNA-expression cassette into their DNA. The cassette prompted the chickens to produce a hairpin-shaped piece of RNA that essentially tricks a viral enzyme known as polymerase into biding with it, rather than the native viral genome. This renders the enzyme useless and prevents the virus from replicating itself. (more…)

Humans are the only living things that cry when they are overcome with emotion. Why do we do this?

A study by Noam Sobel and colleagues at the Weizmann Institute provide part of the answer, at least as it relates to women. The scientists showed that when men get a whiff of women’s tears, they experience a temporary, generalized loss of libido and a dip in testosterone. Really.

(And you thought that red, runny nose was the turn-off, didn’t you?)

Scientists have known for decades that the chemical composition of “emotional tears” differs from tears shed due to simple irritation. But now, it appears that some of the chemicals contained in the former are actually pheromones; biological substances that create behavioral changes in others who are exposed to them. Such chemicals were known to exist in urine in anogenital gland secretions (dont ask), but not in tears.

Sobel’s team began its study by posting ads on Israeli college campus bulletin boards in which they sought volunteers who cried easily. Seventy-one people responded. All but one were women. From that group, the scientists identified 6 who were, like, seriously profuse criers and who could return to their labs every other day.

The scientists then asked each one to select a movie that was guaranteed to make them break down, to watch it in private, and to collect their tears in a vial. For the controls, Sobel’s group trickled a saline solution down the same women’s cheeks and collected that.

Sobel’s group subsequently asked male volunteers to sniff the contents of the 2 vials and ran a battery of psychological and physiological tests to measure their responses.

The men could not distinguish the odorless, colorless liquids, but boy oh boy did their responses differ! In one study, men rated women in photos as less sexually attractive after sniffing “emotional tears” than after they sniffed the saline solution. In another study, men watched scenes from a sad movie after sniffing either the real stuff or saline. They were equally sad regardless of which mixture they sniffed, but the tear-sniffers had lower sexual arousal and lower testosterone levels. (more…)

One year ago, researchers at the National Cancer Institute published a paper that linked Chronic Fatigue Syndrome with an obscure retrovirus known as XMRV. The article caused a stir because 4% of the supposedly healthy people in the study were infected with the virus. That could mean nearly 12 million Americans are infected with a poorly understood virus that potentially causes a poorly understood disease.

There has followed a mad dash to commercialize a blood test for XMRV, since arguably, the nation’s blood supply needs to be screened for the virus. Unfortunately, progress on this endeavor has been slow.

Like HIV-the virus that causes AIDS-XMRV is a retrovirus. XMRV has also been associated with prostate cancer, although no one really knows whether the virus causes diseases of any kind in humans.

Labs involved the effort to develop an XMRV blood test include those at the CDC and the National Cancer Institute, as well private sector programs at Roche, Abbott and Gen-Probe.

Scientists at Abbott are working with the Cleveland Clinic and Emory University. They have created unequivocally positive blood samples from monkeys that were deliberately infected with XMRV. The infected monkeys produced antibodies to 3 proteins on the surface of the virus, but blood levels of these antibodies became undetectabe within weeks after the infection. Tests based on these antibodies can therefore generate false negative results. False negative results can also be caused by the unusually long delay between the time the monkeys were infected with the virus and the time the antibodies appeared.

Even if these issues can be overcome and the antibody test subsequently proven to be useful on human blood, there would remain additional challenges in commercializing the test. For example, the elapsed time between when the blood is obtained and when it is tested could impact test results.

“When there is a new agent that we don’t know a lot about, it’s always a process,” Michael Busch lamented in an interview with the Wall Street Journal. Bush is the director of San Francisco’s Blood Systems Research Institute and a participant in the working group tasked by the Feds to study the potential impact of XMRV on the nation’s blood supply.

Final Thought: It’s hard to criticize a proactive effort to commercialize a blood test for a virus that could be contaminating our nation’s blood supply, but it sure would be nice to know that XMRV actually causes human disease, and that it actually can be transmitted through a blood transfusion. #CartBeforeTheHorse?

Boston University scientists claim to have identified a small set of genetic variants that predicts extreme longevity.

The scientists, Paola Sebastiani and Thomas Perls, examined the DNA of 1,055 centenarians living in New England. They isolated 150 gene variants that were common in this population. They subsequently examined a separate sample of centenarians and found that 77% of them had many of the same genetic variants.

The centenarians in the original cohort had as many disease-associated gene variants as shorter-lived people, so the scientists reasoned that the genes they identified must protect against disease.

This conclusion is at odds with current thinking about extreme longevity which is predicated on the assumption that long life is caused by the absence of disease-causing gene variants, rather than the presence of protective genes.

To find the protective genes, the scientists implemented a genome-wide association study, a technique that has so far failed to meet expectations that it would unlock genetic secrets behind common conditions like diabetes and Alzheimer’s disease.

Some scientists questioned the findings of the BU group. Kari Stefansson, a geneticist who works for Decode Gentics told the New York Times for example, that he was “amazed at how many loci of genome-wide significance have been found in a modest sample size.”

Stefansson’s company has also studied extreme longevity. Apparently, none of the BU group’s 150 genetic variants showed up in the population studied by Decode Genetics.

There are roughly 80,000 centenarians in the US right now. Roughly 15 % of the general population has some or many of the 150 genetic variants found in the BU study. Most of them fail to reach a ripe old age because of accidents or an unhealthy lifestyle.

Their report appears in Thursday’s issue of Science.

The dream of an effective vaccine against the AIDS virus may have moved one step closer to reality, according to federal scientists.

The scientists identified 2 naturally occurring antibodies that destroy nearly 90% of all strains of HIV, the virus that causes AIDS. They say their finding could hasten development of new HIV treatments as well as a vaccine.

HIV is deviously mutable. Frequent mutations in its DNA change the composition of surface proteins on the virus, allowing it to escape an immune response. This enables the virus to continue infecting cells even after antibodies targeting it have appeared — it has thus been able to avoid vaccines developed against it so far.

There are hundreds of variants of the HIV virus around the world. Finding so-called broadly neutralizing antibodies that can kill the majority of these strains has been the goal of HIV researchers for 2 decades.

To date, the best researchers have been able to do is find antibodies that block about 40% of the known HIV strains. Key to a breakthrough in this regard is to isolate antibodies that attack relatively unchanging parts on the surface of the HIV virus. And that’s what may just have been accomplished.

“I am more optimistic about an AIDS vaccine at this point in time than I have been probably in the last 10 years,” Gary Nabel of the National Institute of Allergy and Infectious Diseases told the LA Times. Nabel headed the project reporting the breakthrough. The write-up appears in Science.

Nabel’s team isolated antibodies from a 60-year-old African American man that had been infected with HIV. Using new imaging and analytical techniques, the team isolated 2 antibodies, known as VRC01 and VRC02, which are directed against a protuberance on the surface of the HIV virus. The spike facilitates binding to something called the CD4 binding site on white blood cells of humans. When an antibody binds to to the spike, it prevents the virus from entering the cell.

The HIV virus relies exclusively on this receptor to enter human white blood cells, so it can’t infect them when antibodies are attached to the spike.

Nabel’s team is currently testing a synthetic version of the spike as a possible vaccine in animals. They hope to begin human testing fairly soon.

Boston University scientists claim to have identified a small set of genetic variants that accurately predicts extreme longevity in humans.

The scientists, Paola Sebastiani and Thomas Perls, examined the DNA of 1,055 centenarians living in New England. They isolated 150 gene variants that were common in this population. They subsequently examined a separate sample of centenarians and found that 77% of them had many of the same genetic variants.

The centenarians in the original cohort had as many disease-associated gene variants as shorter-lived people, so the scientists reasoned that the genes they had identified must protect against disease.

This conclusion is at odds with current thinking about extreme longevity which is predicated on the assumption that long life is caused by the absence of disease-causing gene variants, rather than the presence of protective genes.

To find the protective genes, the scientists implemented a genome-wide association study, a technique that had previously failed to meet expectations that it could unlock genetic secrets behind common conditions like diabetes and Alzheimer’s disease.

Some scientists questioned the findings of the BU group. Kari Stefansson, a geneticist who works for Decode Gentics, told the New York Times for example that he was “amazed at how many loci of genome-wide significance have been found in a modest sample size.”

Stefansson’s company has also studied extreme longevity. Apparently, none of the BU group’s 150 genetic variants showed up in the population studied by Decode Genetics.

There are roughly 80,000 centenarians in the US right now. Roughly 15 % of the general population has some or many of the 150 genetic variants found in the BU study. Most of them fail to reach extreme old age because of accidents or an unhealthy lifestyle.

The report appears in Science.

In a truly remarkable scientific breakthrough, researchers at Synthetic Genomics, Inc. have created a living organism that is wholly controlled by man-made genetic instructions.

“We call it the first synthetic cell,” Craig Venter, the company founder who oversaw the project told the Wall Street Journal. “These are very much real cells.”

The unicellular organism can reproduce but has no living ancestors.

The laboratory methods used to create it, which are patented by Synthetic Genomics, appear to be applicable to other bacterial strains with commercial potential. In fact at least 3 companies are using similar methods to create organisms which produce fuels and vaccines and (better late than never) gobble up oil spills.

“This is literally a turning point in the relationship between man and nature,” said molecular biologist Richard Ebright of Rutgers University. “For the first time, someone has generated an entire artificial cell with predetermined properties.”

Synthetic Genomics provided $30 million to fund the work. It owns intellectual-property rights to the entire process.

To create the new life form, Venter and bioengineer Daniel Gibson stripped out the DNA of a bacterium known as Mycoplasma capricolum and replaced it with a genome they built which was a variant of a second species known as Mycoplasma mycoides. The minor variations amount to biochemical signatures of the scientists, essentially proving the creation was theirs.

“We make a genome from four bottles of chemicals; we put that synthetic genome into a cell; that synthetic genome takes over the cell,” Gibson told the Journal. “The cell is entirely controlled by that new genome.”

The incredible work is documented in Science.

Soon after the announcement, the House Energy and Commerce Committee said it would hold public hearings on the matter in the near future.

Scientists have identified a single-gene mutation that enables people to function effectively with far less sleep than most, a discovery that could lead to improved understanding of sleep cycles and open up new paths toward the treatment of insomnia and other sleep disorders.

Ying-Hui Fu and colleagues at UCSF made the find while conducting routine DNA screening on blood samples from people that had participated in several sleep studies.

The scientists had been searching for gene variations that affect circadian rhythms and other aspects of the sleep cycle. When they identified 2 specimens having unusual mutations of the so-called DEC2 gene, they traced them back and found a mother and daughter who routinely functioned on 6 hours of sleep per night. The average requirement is 8 to 8.5 hours per night.

The scientists then bred mice to have the same mutation, and found they required less sleep and recovered more easily from experimental sleep deprivation than regular mice.

The study “opens up a window to understanding the genetic basis of individual differences in sleep duration. You have a piece of the puzzle and you can begin trace back,” Charles Czeisler told the New York Times. He’s chief of sleep medicine at Brigham and Women’s Hospital.

The 2 women turn in around 10 or 10:30 each night and wake up ready to rock and roll at 4 or 4:30 in the morning, according to Fu.

Many people sleep for six or fewer hours per night, but have to use stimulants and alarm clocks to pull off the feat. “That’s a very different thing,” Fu told the Times. “Our body needs 8 to 8.5 hours.” (more…)

Reporting in Science on interim results from a study that began 20 years ago, University of Wisconsin scientists have concluded that rhesus monkeys placed on a calorie-restricted diet live longer than controls receiving a normal diet.

In the study by Ricki Colman and Richard Weindruch, monkeys between the ages of 6 and 14 were randomized to receive a normal diet or one that contained adequate nutritional ingredients but 30% fewer calories.

The svelte monkeys, it turned out, had significantly less risk of developing diabetes, cancer and cardiac disease. And their mortality rate from conditions usually associated with senescence was 13% compared with 37% for those on the normal diet.

“Caloric restriction slows aging in a primate species,” declared the scientists. The results make “it more likely it would apply to humans,” added Weindruch in an interview with the New York Times.

Weindruch estimated the dieting monkeys would live 10-20% longer based on extrapolations from  studies in mice.

Many scientists criticized the study, since a lot of dieting monkeys died of conditions not usually associated with aging (such as endometriosis, complications from anesthesia or gastric bloat). If these deaths were included, the mortality difference between the groups was not significant. 

“The results seem pretty inconclusive at this point,” said Steven Austad, an expert on aging at the University of Texas. “I don’t know why they didn’t wait longer to publish.”

Weindruch wasn’t looking back, however. After all, his monkeys didn’t begin calorie restriction until they were young adults. In mice, even more striking extensions of life occur when dieting begins at birth.

It’s another matter of course, whether rhesus monkeys, if given the option, would choose to adhere to such a diet forever.

Scientists at Stockholm’s Karolinska Institute have proved that the human heart produces new muscle cells throughout normal adult life, raising hope that this regenerative prowess can be harnessed to replace cardiac tissue that had been damaged by heart attacks and other pathological conditions.

Conventional wisdom had been that the heart does not produce new cells and people died with pretty much the same ticker as the one they started out with.

But Jonas Frisen and colleagues determined that up to age 25, the heart replaces about 1% of its cells per year, and it continues doing so, albeit at gradually diminishing rates, through old age.

When it’s all said and done, nearly half the heart’s muscle cells are created during a normal lifetime, the scientists estimated.

The scientists knew that cell turnover rates could be quantified in animals by adding radioactive molecules to cells and observing how quickly the radioactivity disappears.

This can’t be done in humans for ethical reasons, but Frisen reasoned that above-ground nuclear weapons testing, which was done by several countries until 1963, had seeded the atmosphere with carbon-14, and this stuff would find its way into the food chain.

The net result would be that the DNA in the nuclei of all living creatures has been C-14 labeled more or less continually as a byproduct of the nuclear folly.

The C-14 remains in the cell for as long as it survives, but since C-14 levels have diminished since 1963, cellular loads of the stuff in more recently formed cells have also diminished. The amount of C-14 in a particular cell thus indicates when it was formed.

The clever work appears in Science.

Loren Field, a cardiologist at Indiana University, told the New York Times the goal now becomes “to try to tickle the system to enhance (cellular regeneration rates).”