a vaccine for HIV/AIDS on humans.

The approval from the Food and Drug Administration will lead to further tests that, if successful, could see a vaccine on the market in about five years, researchers from the University of Western Ontario said in announcing the milestone Tuesday morning at the campus in London. Ont.

The vaccine is the first based on a genetically modified, killed whole virus, following a line of research that successfully produced vaccines for polio, rabies and hepatitis A.

It is the only HIV vaccine currently under development in Canada, and one of only a few in the world, said the researchers.

Dr. Chil-Yong Kang and a team at the university, funded by pharmaceutical venture company Sumagen Canada, said approval by the American agency was crucial because its strict standards are generally regarded as a world standard.

A clinical trial on 40 HIV-positive volunteers will begin next month.

Those trials will be followed by tests on 6,600 HIV-negative but high-risk-category volunteers, testing immune responses and effectiveness of the vaccine in two more phases.

"I feel happy and comfortable with this human clinical trial," Kang told university and political leaders gathered for the announcement Tuesday.

Kang said the vaccine is being produced at special "bio-safety level 3" laboratories in Maryland and Colorado because there is no suitable lab in Canada.

Three earlier attempts at developing similar vaccines have failed since 2003.

Unlike other research, the Western team uses viruses it kills and genetically modifies to make them safe. Part of that process involves using white blood cells and the melittin protein from honeybees to help cultivate the vaccine.

Other attempts have used live viruses, because research found that route was successful in developing vaccines to combat mumps, measles and smallpox.

Kang said researchers in London had to conduct 230 different tests to satisfy the FDA, some involving primates, to ensure the vaccine would be safe to use on humans.

Sumagen Canada has secured patents to the vaccine in more than 70 countries.

HIV/AIDS has killed more than 28 million people worldwide, and more than 35 million people currently live with the virus that attacks the immune system. Since the virus was characterized in 1983, there have been numerous trials through pharmaceutical companies and academic institutions around the world to develop vaccines; however, no commercialized vaccine has been developed to date.

About the vaccine:

- Attempts to develop a vaccine in 2003, 2007 and 2009 failed.

- Western's is a new approach, similar to that used to develop vaccines for polio, influenza, rabies, hepatitis A, Japanese encephalitis for humans and 16 vaccines to prevent viral diseases in animals.

- The approach uses human immunodeficiency viruses that are killed, then genetically modified to be safe and cultivated with protein from honeybees.

I found this article particularly interesting, hope you like it also.

via:techcrunch

So, this isn’t exactly breaking news, but it’s so awesome that it’s worth sharing again in case you missed it. HIV/AIDS has killed some 25 million people worldwide and scientists have been working diligently since the virus was discovered in 1981 to find a cure. While a cure still eludes researchers, several protease inhibitors have been developed to slow its progress. But last week, HIV/AIDS research took a huge leap forward, thanks to the work of gamers. Yes, gamers.

About three years ago, a team of researchers at the University of Washington created a game called FoldIt to allow gamers to contribute to scientific research by playing with the shape and structure of proteins. Why proteins? Well, there are more than 100,000 kinds of protein in the human body, and understanding the structure and makeup of these proteins is key to understanding how they work and as well as to designing drugs that target them.

As proteins are found in the majority of diseases we suffer from, they are also key to developing cures, and so FoldIt enables gamers to design new proteins and fold known proteins into their most workable forms in an effort to contribute to disease prevention.

According to FoldIt’s website, “Foldit attempts to predict the structure of a protein by taking advantage of humans’ puzzle-solving intuitions and having people play competitively to fold the best proteins”.

And last week, FoldIt became more than just a cool idea, or an exercise for scientifically-minded gamers. Scientists have been attempting to decipher a protein called “retroviral protease” for over 15 years, as the protease is one of the key proteins that allows HIV to multiply and replicate itself in living cells. Using FoldIt, gamers were able to identify the structure of the protein — within a matter of 10 days.

With the structure of retroviral protease unlocked, scientists can now begin taking the necessary steps to build a drug that could significantly slow the speed at which HIV develops. The findings were initially published in a Nature article, which readers can find here.

“Following the failure of a wide range of attempts to solve the crystal structure of M-PMV retroviral protease by molecular replacement, we challenged players of the protein folding game Foldit to produce accurate models of the protein”, the University of Washington research team said in its findings. “Remarkably, Foldit players were able to generate models of sufficient quality for successful molecular replacement and subsequent structure determination. The refined structure provides new insights for the design of antiretroviral drugs”.

In this MSNBC report, the gamers describe the way in which they were able to work together cooperatively to solve a puzzle that has confounded scientists for more than a decade. And what’s so cool is that, while some of the most important progress in the game was made by those with biomedical academic backgrounds, the majority of active players playing with FoldIt did not have this kind of scientific background. Many of them were just average gamers like you and I.

“The monkey-virus puzzle solution demonstrates that Foldit and other science-oriented video games could be used to address a wide range of other scientific challenges — ranging from drug development to genetic engineering for future biofuels”, Firas Khatib, a biochemist at the University of Washington told MSNBC. “My hope is that scientists will see this research and give us more of those cases”.

What a remarkable win for the non-shallow end of gamification. We hear so much about how game layers are being added to consumer tech products to encourage engagement and interaction with products and apps, but with FoldIt, we have a real example of how gamification can help solve some of the trickiest of scientific problems and help make the world a better place.

• By Maryn McKenna

This Sunday — June 5, 2011 — marks what public health considers the 30th anniversary of the international epidemic of HIV-AIDS.

If you’d like a summation of the past 30 years, Larry Altman, the retired senior medical writer of the New York Times, did an excellent job last Tuesday. And the Centers for Disease Control and Prevention summed up, in a paper released at noon ET, the state of the epidemic today.

I was not yet a reporter when the plague began, so my memories of that time are not professional memories, but personal. I was a student, studying mostly theatre, and almost all my friends were gay. And suddenly my friends were dying. People who remember will know what I mean. We got used to seeing people we worked and drank with looking, abruptly, like famine victims. We grew battlefield-numb bringing meals, and attending memorials, and calling people’s mothers on their death anniversaries. We knew when the multi-drug cocktails that changed the course of the epidemic had arrived, not because we read the journal articles, but because suddenly we could take our florists off our speed-dial.

I worry, in the complacency that has settled now around HIV as an almost-chronic illness, that the stunning initial impact of this disease that changed the planet has been somehow forgotten. So for my next three posts, I’m going to take you back to those days.

A few years ago, I wrote a book chronicling the history of the Epidemic Intelligence Service, the young disease-detective corps of the CDC. EIS officers, as they’re called, were in on every major disease event of the last half of the 20th century: the end of smallpox, the beginning of the end of polio. And though his name was never well-known and has been almost forgotten, one of them alerted the world to the first known cases of AIDS.

His name was Wayne X. Shandera, and the anniversary that we’ll mark on Sunday is actually the 30th anniversary of the publication of his urgent bulletin, the first in any medical journal to describe a case of HIV.

Below is Chapter 6 of Beating Back the Devil. We begin in California, in the winter of 1980, where Wayne Shandera is contemplating his options for his 2-year stint in the EIS.

AIDS: 1981, Los Angeles (Part One)

Los Angeles was just about the last place Wayne X. Shandera wanted to end up.

The wiry-haired physician had gone to college at Rice University in Houston, crossed the country to medical school at Johns Hopkins University in Baltimore, and then crossed back for residency at Stanford University outside San Francisco. Now he was wondering whether to pack up again. He had been admitted to the Epidemic Intelligence Service, and the group had asked him to list his preferences for an assignment.

Shandera was 29 years old, a devout Catholic who read three languages and was an accomplished organist. He loved living in the Bay Area; he liked the climate and the architecture, and he felt at home in the left-leaning discourse that simmered in its bookstores and coffee shops. Shandera had moved to San Francisco in 1977, the year that activist Harvey Milk was elected to the city’s board of supervisors. Milk was the first openly gay man to win a popular election anywhere in America. When he was murdered a year later, gay men poured into the city, transforming its colorful, casual decadence into a nexus of sexual flamboyance and political fury. But Shandera had little contact with gay San Francisco. Heterosexual, socially conservative and somewhat shy, he would rather have gone to a chamber music concert than a Pride parade.

At the moment, he was unsure where to go. Conventional CDC wisdom held that headquarters offered the best EIS assignments. Atlanta made personal sense as well. Shandera’s father was ill with colon cancer in San Antonio, and he had left the promising beginnings of a relationship behind in Baltimore three years before. In Atlanta, he thought, he would have easy airplane access in both directions.

On the other hand, he had just finished three years of caring for patients. He had not had a course in statistics or epidemiology since his second year of medical school, and he was weak in the necessary skills of sleuthing out the details of outbreaks and writing coherent narratives about them. He might, he thought, get more practice in a city or state health department. EIS matching lets candidates list up to 10 choices. Shandera studied the list of possible postings and put the Louisiana health department first, followed by eight jobs in Atlanta, and the Los Angeles County health department dead last. It was a low probability, he thought; the matchers never worked their way that far down a candidate’s list.

In June 1980, the notice arrived: After training in Atlanta, Shandera was to pack up his Stanford apartment and move south to Los Angeles.

He was horrified. His colleagues were dismissive.

“You’re not going to find anything to work on there,” his cardiology professor said. “Except for a bunch of sexually transmitted diseases.”

He had no idea how prophetic a statement that was.

-  -  -

It looked, at first, as though Shandera’s derisive professor had been wrong. There were plenty of diseases in Los Angeles. There was a cluster of miscarriages in Long Beach; two outbreaks of diarrhea, one in a day care center and one spread throughout the city; a set of hepatitis cases among women who donated blood plasma; and a puzzling outbreak of epidemic neuromyasthenia, a syndrome of headache, fever and muscle weakness, among patients of a neurologist in Pacific Palisades.

He did not solve all of the outbreaks, though they kept him busy. He worked hard, but he was unhappy. Nothing he was doing seemed novel, and he had been attracted to the EIS by the hope that he could help identify new health problems.

Twice in the past five years, the group’s members had helped identify previously unrecognized diseases. In the summer of 1976, they had scrambled to an epidemic of pneumonia that sickened 221 people and killed 34 at an American Legion convention in a hotel in Philadelphia; by the end of the year, CDC scientists had identified the pathogen causing it, dubbed it Legionnaires’ disease, and exposed it as the cause of two other, never-solved outbreaks in 1965 and 1968. Two months before Shandera joined the EIS, in May 1980, the CDC had linked 55 severe cases of fever, rash and Group A Streptococcusinfection, a constellation of symptoms dubbed toxic shock syndrome, to women’s use of high-absorbency tampons. Nothing that he was seeing in Los Angeles promised the excitement of those discoveries.

He worried, too, that he wasn’t learning enough epidemiology. He missed the intense supervision of residency. He had chosen public health, to start with, out of a sense that he wanted to make more of a difference than he would working one-on-one with patients in a hospital. In Los Angeles, he couldn’t see any evidence that he was making much of a difference at all.

The clincher was that he loathed the place. In San Francisco, he had biked everywhere; now he owned an old Mustang and was immersed every day in the city’s desperate traffic. The air quality was very bad that year — “Some days we couldn’t see across the street,” said Frank Sorvillo, an epidemiologist who shared a cubicle with him — and the frank materialism of the city grated on Shandera’s sensibilities.

“In one day, I would see 20 migrant workers living in a garage in East L.A., and then have to drive through Bel Air and be staggered by the contrasts,” he said. “It was disturbing, and hard to work in. I was at odds with the city most of the time.”

In the spring, Shandera asked the corps to transfer him. They offered him a job in Atlanta, starting in a few months: late July 1981. He accepted.

-  -  -

There was something percolating through Southern California that spring.

Some of the health department’s epidemiologists heard reports from doctors they knew, that patients in practices in the San Fernando Valley were complaining of swollen lymph nodes and stubborn low-grade fevers. There was no obvious diagnosis. Those symptoms could signal the start of lymphoma, a cancer of the immune system that attacks a particular type of white blood cell, but tests were finding no trace of cancer.

Most of the patients, the doctors said, were men.

At about the same time, a pathologist at the University of Southern California called Shandera’s cubicle-mate Frank Sorvillo. He had evidence of cancers in a cluster of six male patients. But there was something odd about what he was seeing through the microscope; the pathology of these lymphomas was like nothing he knew.

One of the patients was still in the hospital, and Shandera and Sorvillo went to interview him. The man was a drug addict, but there was nothing else extraordinary about him, nothing that would predispose him to an unusual lymphatic cancer. They let the case go.

At University of California-Los Angeles, anomalous cases were showing up as well. They were finding their way to Dr. Michael S. Gottlieb, an assistant professor of immunology who had joined the medical school staff in the summer of 1980. Like Shandera, Gottlieb had come from Stanford and they had known each other there slightly. Gottlieb was four years older, and had been a research fellow when Shandera rotated through immunology as a resident; he had gone over cases and journal articles with the younger doctor.

Gottlieb’s specialty was the immunology of organ transplantation. At Stanford, he had looked for ways to persuade the body to accept transplants without using drugs to suppress the immune system, the only way known to keep organs from being rejected as foreign. Unlike Shandera, Gottlieb liked Los Angeles. While at Stanford, he spent some time at UCLA studying bone-marrow transplants, and the university invited him to move south and open an immunologic research lab.

Gottlieb was one of the attending physicians — senior doctors who supervise the training of younger ones — on the immunology service of the UCLA School of Medicine. On a slow day in March 1981, he asked Dr. Howard Schanker, a fellow, to patrol the hospital for patients whose cases might present teaching opportunities.

Gottlieb’s office was in the hospital basement. Schanker left for the upper floors. Very shortly afterward, he came back.

“He had a quizzical look on his face,” Gottlieb said. “He said, ‘There is a guy upstairs whose infections are really kind of strange.’”

A very unusual blood transplant appears to have cured an American man living in Berlin of infection with the AIDS virus, but doctors say the approach is not practical for wide use. The man, who is in his 40s, had a blood stem cell transplant in 2007 to treat leukemia. His donor not only was a good blood match but also had a gene mutation that confers natural resistance to HIV.

Now, three years later, the recipient shows no signs of leukemia or HIV infection, according to a report in the journal Blood.

"It's an interesting proof-of-concept that with pretty extraordinary measures a patient could be cured of HIV," but it is far too risky to become standard therapy even if matched donors could be found, said Dr. Michael Saag of the University of Alabama at Birmingham.

He is past chairman of the HIV Medicine Association, an organization of doctors who specialize in treating AIDS.

Transplants of bone marrow — or, more commonly these days, of blood stem cells — are done to treat cancer, and their risks in healthy people are unknown. The transplant involves destroying the person's native immune system with powerful drugs and radiation, then replacing it with donor cells to grow a new immune system. Mortality from the procedure or its complications can be 5 percent or more, Saag said.

"We can't really apply this particular approach to healthy individuals because the risk is just too high," especially when drugs can keep HIV in check in most cases, Saag said. Unless someone with HIV also had cancer, a transplant would not likely be considered, he said.

When the Berlin man's case first surfaced two years ago, Dr. Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases, said the procedure was too expensive and risky to be practical as a cure, but that it might give more clues to using gene therapy or other methods to achieve the same result.

More than half a dozen pornographers in California's multibillion-dollar adult entertainment industry have halted production after an actor tested positive for HIV — and more shutdowns were expected.

Vivid Entertainment Group and Wicked Pictures were among the companies that announced production halts as a precaution.

"From Vivid's perspective, there was no question that when we heard this, we immediately shut down production and said let's get the facts and evaluate them before we move forward," Steven Hirsch, the founder of Vivid, one of the largest makers of adult films, said Wednesday.

"Adult entertainment companies act responsibly, and no one wants to see another person test positive if there's anything they can do to stop it," he said.

Actors in movies by Wicked Pictures use condoms. Still, company president Steve Orenstein said two shoots were on hold and future production depends on further HIV test result from a clinic that serves the industry.

PinkVisual Productions is also slated to halt production for at least a few weeks. Adult Video News reported additional shutdowns at Hustler Video, Digital Playground, Jennaration X Studios, Girlfriends Films and Kick Ass Pictures.

The identity and gender of the HIV-positive actor have not been released by the Adult Industry Medical Healthcare Foundation, which operates the clinic where the case was discovered. The clinic was working to identify and test on-screen partners of the actor.

Los Angeles County public health officials and state occupational health officials have said the widespread lack of condom use on porn sets puts performers at risk of contracting HIV and other diseases. Adult film producers have said viewers find condoms to be a turnoff.

Last year, a woman tested positive for HIV after making an adult film, and in 2004 an HIV outbreak affecting several actors spread panic in the industry and briefly shut down productions at several California studios.

In recent years, advocates and health officials have tussled with porn producers and free speech advocates over the use of condoms in adult films.

State workplace safety officials at Cal/OSHA are considering strengthening rules designed to prevent transmission of disease by requiring the use of condoms in the adult film industry.

Health and workplace safety officials say they have called on the clinic where the case was discovered to share redacted records that would indicate an infected worker's employment history, but the clinic has not complied.

Lawyers for the San Fernando Valley clinic said it was in full compliance with reporting and privacy laws and that health officials have overstepped their bounds in the past.

The lawyers said in a statement Wednesday that a Northern California judge has gone so far as to stop state officials from getting identifying information because it violates medical privacy regulations.

HIV is spread most often through sexual contact but can also be contracted through sharing contaminated needles for drug use, infected blood products, or by babies born to or breast-fed by infected women.

HIV is the cause of AIDS, an immune disease that gradually destroys the body's ability to fight illness.

In an average month, Vivid spends $250,000 to shoot four movies, which require a total of 12 to 15 days of shooting, Hirsch said.

The company currently has a stockpile of unreleased movies, and it would take months without any new production activity to affect Vivid's release schedule, he added.

Mark Kernes, senior editor at Adult Video News, said he expects most production companies to shut down until it's known who had contact with the person known to have HIV.

It's unclear how the industry's bottom line might be affected by halted production because many companies such as Vivid could sustain sales with backlogs of unreleased titles, Kernes said.

Like other entertainment industries, adult filmmakers have been hurt by the recession and the Internet, where pirating and free downloads often cut producers out of a profits.

Last year, in a tongue-in-cheek complaint about the sour economy, Hustler magazine publisher Larry Flynt and Girls Gone Wild chief executive Joe Francis called for a $5 billion federal bailout. They said adult DVD sales and rentals decreased 22%.

Buried deep within each cell in Sergey Brin's body—in a gene called LRRK2, which sits on the 12th chromosome—is a genetic mutation that has been associated with higher rates of Parkinson's.

Several evenings a week, after a day’s work at Google headquarters in Mountain View, California, Sergey Brin drives up the road to a local pool. There, he changes into swim trunks, steps out on a 3-meter springboard, looks at the water below, and dives.

Brin is competent at all four types of springboard diving—forward, back, reverse, and inward. Recently, he’s been working on his twists, which have been something of a struggle. But overall, he’s not bad; in 2006 he competed in the master’s division world championships. (He’s quick to point out he placed sixth out of six in his event.)

The diving is the sort of challenge that Brin, who has also dabbled in yoga, gymnastics, and acrobatics, is drawn to: equal parts physical and mental exertion. “The dive itself is brief but intense,” he says. “You push off really hard and then have to twist right away. It does get your heart rate going.”

There’s another benefit as well: With every dive, Brin gains a little bit of leverage—leverage against a risk, looming somewhere out there, that someday he may develop the neurodegenerative disorder Parkinson’s disease. Buried deep within each cell in Brin’s body—in a gene called LRRK2, which sits on the 12th chromosome—is a genetic mutation that has been associated with higher rates of Parkinson’s.

Not everyone with Parkinson’s has an LRRK2 mutation; nor will everyone with the mutation get the disease. But it does increase the chance that Parkinson’s will emerge sometime in the carrier’s life to between 30 and 75 percent. (By comparison, the risk for an average American is about 1 percent.) Brin himself splits the difference and figures his DNA gives him about 50-50 odds.

That’s where exercise comes in. Parkinson’s is a poorly understood disease, but research has associated a handful of behaviors with lower rates of disease, starting with exercise. One study found that young men who work out have a 60 percent lower risk. Coffee, likewise, has been linked to a reduced risk. For a time, Brin drank a cup or two a day, but he can’t stand the taste of the stuff, so he switched to green tea. (“Most researchers think it’s the caffeine, though they don’t know for sure,” he says.) Cigarette smokers also seem to have a lower chance of developing Parkinson’s, but Brin has not opted to take up the habit. With every pool workout and every cup of tea, he hopes to diminish his odds, to adjust his algorithm by counteracting his DNA with environmental factors.

“This is all off the cuff,” he says, “but let’s say that based on diet, exercise, and so forth, I can get my risk down by half, to about 25 percent.” The steady progress of neuroscience, Brin figures, will cut his risk by around another half—bringing his overall chance of getting Parkinson’s to about 13 percent. It’s all guesswork, mind you, but the way he delivers the numbers and explains his rationale, he is utterly convincing.

Brin, of course, is no ordinary 36-year-old. As half of the duo that founded Google, he’s worth about $15 billion. That bounty provides additional leverage: Since learning that he carries a LRRK2 mutation, Brin has contributed some $50 million to Parkinson’s research, enough, he figures, to “really move the needle.” In light of the uptick in research into drug treatments and possible cures, Brin adjusts his overall risk again, down to “somewhere under 10 percent.” That’s still 10 times the average, but it goes a long way to counterbalancing his genetic predisposition.

It sounds so pragmatic, so obvious, that you can almost miss a striking fact: Many philanthropists have funded research into diseases they themselves have been diagnosed with. But Brin is likely the first who, based on a genetic test, began funding scientific research in the hope of escaping a disease in the first place.

His approach is notable for another reason. This isn’t just another variation on venture philanthropy—the voguish application of business school practices to scientific research. Brin is after a different kind of science altogether. Most Parkinson’s research, like much of medical research, relies on the classic scientific method: hypothesis, analysis, peer review, publication. Brin proposes a different approach, one driven by computational muscle and staggeringly large data sets. It’s a method that draws on his algorithmic sensibility—and Google’s storied faith in computing power—with the aim of accelerating the pace and increasing the potential of scientific research. “Generally the pace of medical research is glacial compared to what I’m used to in the Internet,” Brin says. “We could be looking lots of places and collecting lots of information. And if we see a pattern, that could lead somewhere.”

In other words, Brin is proposing to bypass centuries of scientific epistemology in favor of a more Googley kind of science. He wants to collect data first, then hypothesize, and then find the patterns that lead to answers. And he has the money and the algorithms to do it.

Two common forms of cancer have been genetically mapped for the first time, British scientists announced, in a major breakthrough in understanding the diseases.

The maps have exposed the DNA mutations that lead to skin and lung cancers, in a discovery scientists said could transform the way these diseases are diagnosed and treated in coming years.

All cancers are caused by damage to genes -- mutations in DNA -- that can be triggered by environmental factors such as tobacco smoke, harmful chemicals or ultraviolet radiation, and causes cells to grow out of control.

Scientists from Britain's Wellcome Trust Sanger Institute and their collaborators have mapped this genetic damage from the tumours of two patients suffering from lung cancer and malignant melanoma, a deadly skin cancer.

"This is a fundamental moment in cancer research. From here on in we will think about cancers in a very different way," said Professor Mike Stratton who led the institute's cancer genome project.

"Today for the first time, in two individual cancers, a melanoma and a lung cancer, we have provided the complete list of abnormalities in DNA in each of those two cancers," he told the BBC.

"We now see uncovered all the forces that have generated that cancer and we now see all the genes that are responsible for driving those two cancers."

The scientists' research, published in the journal Nature, also gained deeper insights into the way the body tries to repair the damage caused by the cancers and stop the disease spreading.

Stratton said the research could in future change the way cancers are treated -- by using genetic maps to find the defects that caused them.

"Now that we have these comprehensive complete catalogues of mutations on individual cancers, we will be able to see how each cancer developed, what were the exposures, what were the environmental factors and that's going to be key for our understanding generally of how cancers develop," he said.

"And for our individual patients, we will see all the genes that are abnormal and are driving each cancer and that's really critical, because that will tell us which drugs are likely to have an effect on that particular cancer and which are not."

Peter Campbell, a cancer-genomics expert involved in the research, said the number of mutations discovered -- 33,345 for melanoma -- and 22,910 for lung cancer -- was remarkable.

"It is amazing what you can see in these genomes," he said on the website of the journal Nature.

The research shows most mutations could be traced to the effects of chemicals in tobacco smoke (in the lung tumour) or ultraviolet light (in the melanoma tumour), supporting the idea that they are largely preventable.

"Every pack of cigarettes is like a game of Russian roulette," he said.

"Most of those mutations will land where nothing happens in the genome and won't do major damage, but every once in a while they'll hit a cancer gene."