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In a potential breakthrough in the prevention of AIDS, researchers are reporting today that a vaginal gel containing an existing AIDS drug can cut in half a woman"s chances of getting HIV from an infected partner.

The women involved in the study used it only 60 percent of the time, and it was still effective -- meaning an even greater prevention rate is possible if it"s used more frequently.

The study (PDF here) was published online Monday in Science.

The results still need to be confirmed, and scientists disagree about whether the protection it offers is sufficient to justify using the gel right away. But it"s a major step in the fight to provide women another method besides condoms to protect themselves from infection. It"s especially important in sub-Saharan Africa, where more than two-thirds of the world"s HIV infections occur, according to AP.

Dr. Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases, tells AP the gel marks the first time researchers have seen any microbicide make a statistically significant impact.

The gel was announced at the International AIDS Conference in Vienna, where thousands of scientists, policymakers and activists are gathered. The next few days will include announcements about new drug therapies and genetic research, as well as discussions about funding for research and prevention.

The study involved 900 South African women who were administered a special gel spiked with the AIDS drug tenofovir. The gel cut the risk of HIV infection by 50 percent after one year of use and 39 percent after 2 1/2 years, compared to a gel that contained no medicine, according to the study. The women used the gel only 60 percent of the time, and those who used it more often had higher rates of protection. Scientists say more frequent use is key -- the gel does not need to be changed.

Of the 444 women who received a placebo gel, 60 became infected with HIV, versus 38 infections in the 445 women who received the microbicide, Science Express reports. That"s a statistically significant difference, the researchers say.

The gel is in limited supply, but 99 percent of the women in the study said they"d definitely use it if they knew it prevented the spread of HIV.

[Science, RD Magazine]

For years, every time Vance Vredenburg visited his study area in Kings Canyon National Park in California, he tallied about 100 Sierra Nevada yellow-legged frogs. But in 2005, all the San Francisco State University biologist found were 30 carcasses floating in a lake. Most of the park"s 10,000 frogs had fallen victim to chytrid, a disease that"s the biggest threat to vertebrate biodiversity in history. This summer, Vredenburg returned to the area with plastic tubs full of a bacterial species that might save both this frog and other amphibians around the world.

Chytrid is caused by the fungus Batrachochytrium dendrobatidis, which interferes with an amphibian"s ability to breathe and regulate fluid. No one knows where it came from, but over the past decade it has extinguished 200 of the 6,600 amphibian species found world-wide, and threatens another third. The fungus kills quickly, in some cases wiping out more than 90 percent of an amphibian population within a year.

In the race to find a cure, scientists are turning to an unusual source: amphibian skin. In 2009, biologist Reid Harris of James Madison University and his colleagues discovered that the bacteria Janthinobacterium lividum, found on some yellow-legged frogs" skin, kills the chytrid fungus. to boost this natural protection in frogs, the scientists developed a "bioaugmenting" technique, bathing the amphibians in the bacteria. In laboratory tests, the bacteria conferred full immunity against the chytrid fungus.

Encouraged by these results, Vredenburg wanted to see if the technique would work in the wild. He received rare approval from the national park service to perform an experiment in Kings Canyon, bathing 80 yellow-legged frogs in the protective bacteria and then releasing them. As of last fall, a preliminary rough analysis of data shows that that those treated had about one tenth the fungus levels of those that weren"t. Vredenburg will return this spring to see if the resistance lasts. "If this works," he says, "it could save hundreds of species."

The bioaugmenting technique could work well with the many amphibian species already colonized with low levels of the bacteria. But what about species that lack anti-chytrid bacteria? Saving these animals might mean transferring bacteria between species, and that is a riskier endeavor. Scientists generally warn against introducing non-native species to a new environment, and some believe that moving a bacteria from one frog species to another could be disastrous. In a worst- case scenario, the bacteria could kill other fungi that plants need to survive, destroying the ecosystem and its amphibian residents too.

But many scientists, such as biologist Matthew Becker, who is working to save the Panamanian golden frog, believe that the potential benefits might outweigh the risks. Amphibians play a critical role in connecting freshwater and terrestrial habitats, and they hunt disease-carrying insects. They also produce compounds on their skin that could lead to drugs against HIV and other pathogens.

Becker, a biologist at Virginia Tech, is now using bioaugmentation to try to save the Panamanian golden frog, which is thought to exist only in captivity. The golden frog would die if sent back to its chytrid-tainted home, says Becker. But instead of colonizing it with

J. lividum, which is native only to temperate regions, Becker collected 440 samples from closely related Panamanian amphibians and is testing them to find new bacterial strains native to the area. The hope is that using a bacteria from a similar amphibian will minimize any adverse effects when the animal is reintroduced to its natural habitat.

It"s a race, a matter of striking a balance between the meticulous lab work needed to ensure safety and rescuing frogs before it"s too late. "It made me incredibly nervous to be there with these petri dishes of bacteria. Ideally, I"d do this five years from now after extensive lab studies," Vredenburg says. "But by then, all my frogs would be extinct."

We"re always suckers for a good art/science mashup, so perhaps it"s no surprise that we"re feeling pretty good about today"s release of the 2010 International Science and Engineering Visualization Challenge winners. This year"s winning entries included

the most detailed 3-D model of the HIV virus ever made (above), a sweeping infographic primer on the many ways fungi impact our lives, and a non-interactive media project that tracked 3,000 pieces of garbage from their origins in Seattle to destinations across the U.S.

Click to launch the photo gallery

The competition, sponsored by the journal Science and the National Science Foundation, annually recognizes visualizations that engage viewers by leveraging science in interesting and novel ways. Winners are supposed to exhibit not only originality and artistry, but also an effectiveness at communication scientific ideas and creating awareness.

The winners will be featured in a cover story in an issue of Science publishing tomorrow, but we went ahead and gathered some of our favorites here. Click through the gallery link to see some of the best science imagery the last year had to offer.

[Eurekalert]

Big time news on the fight against AIDS out of Rome today, and it essentially boils down to this: antiretrovirals work (at least, an astoundingly high percentage of the time when they are used correctly). At the biggest forum on HIV and AIDS in the 30-year battle against the deadly epidemic (it still kills 5,000 people a day, FYI), two breakthrough findings show that antiretrovirals (ARVs) not only battle HIV in infected persons, but can stop the disease from spreading in two important ways: it helps prevent HIV-positive folk from transmitting the disease, and also helps prevent non-infected people from contracting it.

A handful of big-time findings were presented, but two stand out. The first major strategy under study, known as "Treatment as Prevention," showed that when HIV-positive people were given an early start on HIV drugs, the chances of their transmitting the virus to their non-infected partners dropped by an astounding 96 percent.

The second major finding goes by the acronym PreP, for pre-exposure prophylaxis. PreP involves giving ARVs to non-infected partners of HIV-positive subjects as opposed to the infected partner. This also works with statistically significant frequency, cutting transmission by 73 percent.

PreP, however, raises ethical issues as well. When some nine million HIV-infected people the world over are in need of daily ARVs, its very tough to justify giving them to those who arent infected just to stem the spread. Which leads us to the crux of the matter: HIV/AIDS prevention needs cash to roll these ARVs out in the field, and right now free cash around the world is on the decline.

Western nations, the major source of this kind of funding, are cutting budgets. Organization like the WHO and the UN, normally the fundraisers for this kind of relief, are tightening the purse strings right at the point when it might be possible to turn back the tide on HIV, which added 2.6 million infected people to its rolls in 2009. Says the AFP: "Just to get 15 million badly-infected people on AIDS drugs by 2015, in line with the newly stated goal by UN members, will require between $22 billion and $24 billion annually."

So as always it comes down to money. But there is hope: Just last week California-based Giliead Sciences inked a deal with the UNs medical patent pool to allow Indian firms that specialize in generic pharmaceuticals to make cheap copies of four leading ARVs for sale in 100 poor countries. And some low doses of ARVs can be offered now in pill form for just 25 cents a day.

[AFP, New Scientist]

Genetically modified glow-in-the-dark cats not only make stylish, futuristic pets, but now provide insight into feline AIDS as well. The cats were injected with an antiviral gene from a rhesus macaque monkey that helps them resist feline AIDS, along with one that produces the fluorescent protein GFP. The latter gene, which is naturally produced by jellyfish, is regularly used in genetic engineering as a way to mark cells. If the cats arent glowing, then the AIDS-resisting gene might not have made it into the cell either.

Infection-fighting proteins called restriction factors, made by both cats and humans, are powerless against their respective versions of AIDS. But monkey versions of restriction factors, like the ones produced by the gene from the rhesus macaque, are able to fight HIV and FIV, as the viruses counter-weapons are designed to fight against human or cat proteins.

The team of American and Japanese scientists injected the antiviral gene and the GFP gene into feline eggs. Almost all of the offspring from these modified eggs had the restriction factor genes, with both fluorescent and AIDS-fighting proteins made throughout their bodies. Cells taken from the animals were found to be resistant to FIV, and the team plans to eventually expose the cats themselves to the virus to see if the restriction factors will protect them. Proof that these genes can protect cats from feline AIDS would be a huge step towards figuring out how to protect humans and prevent HIV.

[BBC]

News from the field of HIV research has been pretty promising of late - this summer, we heard good news that antiretroviral treatment is superbly effective, at least when its used correctly. And thanks to some video gamers, scientists understanding of proteins involved in HIV keeps getting better. Now researchers have another tool in their arsenal: Stripping the virus itself of its ability to trick the human immune system.

HIV infection sends the immune system into overdrive and eventually exhausts it, which is what leads to AIDS. But removing cholesterol from HIV seems to cripple the virus ability to over-activate part of the immune system, so it could potentially lead to a vaccine that lets the adaptive immune system attack and destroy the virus - just as it would if HIV was any other pathogen.

Dr. Adriano Boasso, an immunologist and research fellow at Imperial College London, said keeping the bodys first-responder immune cells quiet could have some benefits - the whole system may not burn out so quickly, and could potentially fight off HIV.

"Think of the immune system as a car. HIV forces the car to stay in first gear, and if you do that too long, the engine is not going to last very long," he said in an interview. "But if we take the cholesterol away, HIV is not capable of attacking the immune system quite as well. Practically, what weve done is turn HIV into a normal jump-start of a car."

Viruses replicate by invading cells and hijacking their machinery, which they use to churn out new copies of their genetic material. Among the repurposed material is cholesterol, which is important in maintaining cellular fluidity, something viruses require to interact with other cells. (This is not related to the way everyone thinks of cholesterol, which is cholesterol in the blood. That type of cholesterol, made of high-density and low-density lipoproteins, is related to heart disease, not HIV and AIDS.)

HIV quickly activates plasmacytoid dendritic cells, or pDCs, which are the first immune cells that respond to the virus. PDCs produce molecules called interferons, which both interfere with the virus replication and also switch on adaptive immune cells, like T cells. Boasso and other researchers believe this hyperactivation weakens the secondary immune system, undermining the bodys ability to respond.

But in a new study, Boasso and colleagues show that removing the cholesterol changes HIV, so that it cannot activate the pDCs like it normally would. By preventing these first responder cells from turning on in the first place, the secondary responders - the T cells - can organize a more effective counterassault.

"Modifying the virus affects the way the immune system sees it," Boasso said. He said its like removing the weapons from HIVs arsenal: "By removing cholesterol, we can turn those little soldiers into an armorless enemy, which can be recognized by the opponents army."

Emily Deal is a postdoctoral fellow at the Gladstone Institute of Virology and Immunology at the University of California-San Francisco. She studies pDC activation in viral infections, and said the cholesterol removal is allowing less of the HIV into the dendritic cells in the first place - which means theres less of the virus for the cells to detect, which leads them to produce fewer interferons.

But keeping the pDCs from turning on could be both good and bad, she said.

"What is better for the host in the long run? Is it better to suppress replication early on, but potentially have some of your T cells die? Or what are the lon-term effects of having replication proceed in the absence of interferons, but have your T cells live?" she said. "Its a complicated system."

Ideally, further studies would look at this give-and-take relationship in monkeys, so researchers could determine if a de-cholesterolized version of HIV could be an effective form of vaccine, she said.

"I think it has a shot," she said. "However, pDCs control a lot of the immune system, and if theyre not getting turned on at all, that may have other effects. If youre trying to use it as a vaccine, it may not induce enough of a response to be protective."

Boasso said the de-cholesterolized HIV could be studied for use in a potential vaccine, but its difficult to stimulate the immune system to fight off an invader when the system itself is the target.

"Theres going to be a lot of work to do," he said.

The study, which also involved researchers at Johns Hopkins University, the University of Milan and Innsbruck University, is published in the journal Blood.

Artificial blood may become a common reality, thanks to the first successful transfusion of lab-grown blood into a human. Luc Douay, of Pierre and Marie Curie University, Paris, extracted hematopoietic stem cells from a volunteers bone marrow, and encouraged these cells to grow into red blood cells with a cocktail of growth factors. Douays team labeled these cultured cells for tracing, and injected 10 billion of them (equalling 2 milliliters of blood) back into the marrow donors body.

After five days, 94 to 100 percent of the blood cells remained circulating in the body. After 26 days, 41 to 63 percent remained, which is a normal survival rate for naturally produced blood cells. The cells functioned just like normal blood cells, effectively carrying oxygen around the body. "He showed that these cells do not have two tails or three horns and survive normally in the body," said Anna Rita Migliaccio of Mount Sinai Medical Center in New York.

This is great news for international health care. "The results show promise that an unlimited blood reserve is within reach," says Douay. The world is in dire need of a blood reserve, even with the rising donor numbers in the developed world. This need is even higher in parts of the world with high HIV infection rates, which have even lower reserves of donor-worthy blood.

Other attempts to synthesize blood have focused on creating an artificial blood substitute, rather than growing natural blood with artificial means. For example, Chris Cooper of the University of Essex in Colchester, UK, is working on a hemoglobin-based blood substitute that is less toxic than the protein in its unbound state. Artificial blood substitutes present a solution for transfusions after natural disasters and in remote areas. The artificial substitutes do not require refrigeration, unlike fresh and stem cell-grown blood.

The stem cell method has its own pros, though. "The advantage of stem cell technology is that the product will much more closely resemble a red cell transfusion, alleviating some of the safety concerns that continue around the use of the current generations of artificial products," says Cooper.

While Douays results, published in the medical journal Blood, are a major step forward, mass-produced artificial blood is still a long way away. A patient in need of a blood transfusion would require 200 times the 10 billion cells that Douay and his colleagues used in the test. Robert Lanza, one of the first people to grow red blood cells in a lab on a large scale, suggests using embryonic stem cells, which could generate 10 times the amount grown by Douay.

[New Scientist]