A CenturiesOld Chinese Herbal Medicine Could Help Us to Fight TB

As science struggles to find new chemicals to address old afflictions, one more time an ancient — and wholly natural — remedy may be the answer, in this case with fighting tuberculosis (TB), according to Science Alert. It turns out that a compound called arteminsinin, which comes from a form of wormwood, not only treats malaria, but antibiotic-resistant TB bacteria.



While the research is ongoing, it adds to the growing body of evidence that Mother Nature more often than not has the solution to common illnesses. Antibiotics are a foundational component of modern medicine, without which many of our current treatment modalities and medical procedures become exceedingly dangerous. But overuse of antibiotics has made them increasingly ineffective against serious infections.

This antibiotic-resistance has turned into a worldwide health threat of massive proportions that kills tens of thousands every year. One infection, Methicillin resistant Staphylococcus aureus (MRSA), kills more Americans each year than the combined total of emphysema, HIV/AIDS, Parkinson’s disease, and homicide. Solutions for this include improved infection prevention, more responsible use of antibiotics in human medicine, limiting use of antibiotics in agriculture, and finding innovative approaches to treat infections.

But in the wake of this crisis, a good thing has emerged: the re-discovery of natural infection-fighting methods. From garlic to cinnamon to probiotics and fermented foods, to sunlight and Manuka honey, there are positive things in nature that are turning out to be good combatants for fighting infections.

Manuka honey has even been shown to be more effective than antibiotics in the treatment of more than 250 clinical strains of bacteria as well as serious, hard-to-heal, antibiotic-resistant skin infections, including MRSA.

Did Dr.Robert Gallo Create HIV/AIDS?

A site run by a friendly and reasonably honest woman I know recently reposted a text titled “The Man Who Created AIDS: Robert Gallo.” The text went super-viral, over 80,000 shares on Facebook alone. Once I read it, I was aghast at how much misinformation and how many scientifically illiterate statements were in the text and attached video. I wrote her explaining my reasoning, and she immediately agreed to take down the text. It still exists on other, less responsible, sites.


Robert Gallo, discoverer, and alledged creator, of HIV

Unfortunately, a large part of the damage has already been done, and that among other articles has helped foster the continued existence of a completely unfounded theory based primarily on not understanding what a patent is in molecular biology.

A patent on Ebola or HIV is not the same as a patent on an engine. Whereas the engine’s patent is reserving the production of that type of engine to the patent holder, a patent on HIV or Ebola is a patent meant to specify how the virus was isolated, how the genotype was determined, and what this consensus genotype is. In biology, you can patent things you found to concretely identify that component, potentially for use in a more complex system later. Keep in mind that you can even patent seeds obtained from cross-pollination: the patent does not mean the species was genetically modified in a laboratory.

The same way a patent on cross-bred species does not mean it was created in a lab, a patent on a virus genome does NOT mean it was created in a lab. Robert Gallo first published his isolation and identification of HIV in 1984, and patented this in 1985.  After older blood samples were then analysed in a search for this virus, it was then found in the past: it didn’t suddenly occur in the 1970s or 1980s.

Despite the claims of the article whose damage I am working to undo, the earliest samples of HIV positive blood did not originate from New York homosexuals from the 1970s, but insteaddate back to 1920s Congo. The virus most certainly did not originate from biological weapons programs, which are only today becoming advanced enough that creating such a virus is even theoretically possible. They were most certainly not advanced enough in 1920, or even 1960, to create a synthetic retrovirus, which I might add, has still never actually been accomplished.

One of the articles I saw blaming Gallo comically claims that chimps were supposedly deliberately infected and released in 1979, which somehow led to the virus occurring in New York in 1971. The viral “Gallo did it” article that I convinced my friend to take down had anembedded video, where a man “explains” over dramatic music that HIV was created through “combining lymphoma, leukemia, and carcinoma viruses.” I literally burst out laughing, because none of what he listed was a retrovirus or even a virus, and cancer has literally nothing to do with HIV. You could spend your entire life combining lymphomas, carcinomas, and leukemia, and you would still never end up with a retrovirus at the end.

All of these theories make very specific claims, without any evidence. They encourage me to believe that a man (who thinks cancers are viruses) has special knowledge and access to untold classified documents. To prove his point, the video displays extremely blurry documents that are barely legible beyond seeing Gallo’s name. For all we know, these documents are completely fake, or actually completely harmless. We don’t know, because as is the norm in such articles or videos: no sources are supplied.

Yes, the United States did and maybe still does have biological weapons programs. The Soviets did, and Russia still runs its “Vector” high-security lab, as well. This is absolutely no indication that HIV is a bioweapon, especially considering the actual time-line of infections. There are even more reasons why Ebola is certainly not a bioweapon, but that is beyond the scope of this text. Gallo was a scientist, and a researcher, and his position in the public eye is yet another reason to doubt him being an evil mastermind.

There is no historical evidence actually implicating Gallo, or any others, in creating a HIV virus.  All of the historical and scientific evidence, as well as a general understanding of patents in science, point to a legitimate researcher, along with his peers, simply trying to identify understand a human illness. There may very well be one or more synthetic doomsday viruses sitting snugly or being worked on in undisclosed locations (or in BSL-4 labs), but HIV and Ebola are not examples of this.

Latent HIV Reservoir May Be Larger Than Previous Estimates

The sleeping giant of HIV infection—a reservoir of viral DNA that lies dormant in human immune cells—could be far larger than previously believed.

A study published today in the journal Cell shows that the reservoir, consisting of proviruses integrated into resting CD4 immune cells, may be 60 times larger than scientists had estimated. Antiretroviral therapy (ART) kills replicating HIV but not the latent proviruses, which pose a major barrier to eradicating the virus from the body and curing infection.

The latent HIV reservoir in people who are infected could be 60 times larger than previously estimated, according to a new study. Image:  JAMA, ©AMA

Recent research had indicated that fewer than 1% of proviruses become infectious when resting CD4 cells are activated in a test tube. Without activation, proviruses can’t replicate. The proviruses that don’t cause infection have been considered defective, but investigators hadn’t described specifics about the deficiencies.

In the new study, a team of investigators used a more detailed method to study proviruses that didn’t switch on and become infectious when the resting CD4 cells they inhabited were activated in the laboratory. They cloned the genomes of 213 inactive proviruses from 8 HIV-infected patients treated with ART for more than 6 months. Their genetic analyses showed that about 88% of proviruses that didn’t turn on had obvious defects that prevented them from replicating. But nearly 12%—a far greater percentage than previously estimated—were capable of replicating and causing infection.

The investigators said their study suggests that there are enough proviruses that don’t turn on but are capable of replicating to boost the size of the latent reservoir by 60-fold. “These results indicate an increased barrier to cure, as all intact noninduced proviruses need to be eradicated,” senior author Robert Siliciano, MD, PhD, of Johns Hopkins University School of Medicine in Baltimore, said in a statement.

“We would like to use these findings by developing better ways to measure the size of the latent reservoir in patients who are participating in future trials of potentially curative strategies,” Siliciano added. “In this way, we think our analysis will contribute to HIV eradication efforts.”

World AIDS Day: The Photo That Changed the Face of HIV/AIDS

LIFE.com shares the story behind one of the most harrowing and controversial photographs to emerge from the global pandemic

In November 1990 LIFE magazine published a photograph of a young man named David Kirby — his body wasted by AIDS, his gaze locked on something beyond this world — surrounded by anguished family members as he took his last breaths. The haunting image of Kirby on his death bed, taken by a journalism student named Therese Frare, quickly became the one photograph most powerfully identified with the HIV/AIDS epidemic that, by then, had seen millions of people infected (many of them unknowingly) around the globe.

Here, a quarter-century later, LIFE.com shares the deeply moving story behind that picture, along with Frare’s own memories of those harrowing, transformative years.

“I started grad school at Ohio University in Athens in January 1990,” Frare told LIFE.com. “Right away, I began volunteering at the Pater Noster House, an AIDS hospice in Columbus. In March I started taking photos there and got to know the staff — and one volunteer, in particular, named Peta — who were caring for David and the other patients.”

David Kirby was born and raised in a small town in Ohio. A gay activist in the 1980s, he learned in the late Eighties — while he was living in California and estranged from his family — that he had contracted HIV. He got in touch with his parents and asked if he could come home; he wanted, he said, to die with his family around him. The Kirbys welcomed their son back.

Peta, for his part, was an extraordinary (and sometimes extraordinarily difficult) character. Born Patrick Church, Peta was “half-Native American and half-White,” Frare says, “a caregiver and a client at Pater Noster, a person who rode the line between genders and one of the most amazing people I’ve ever met.”

“On the day David died, I was visiting Peta,” Frare, who today lives and works in Seattle, told LIFE. “Some of the staff came in to get Peta so he could be with David, and he took me with him. I stayed outside David’s room, minding my own business, when David’s mom came out and told me that the family wanted me to photograph people saying their final goodbyes. I went in and stood quietly in the corner, barely moving, watching and photographing the scene. Afterwards I knew, I absolutelyknew, that something truly incredible had unfolded in that room, right in front of me.”

“Early on,” Frare says of her time at Pater Noster House, “I asked David if he minded me taking pictures, and he said, ‘That’s fine, as long as it’s not for personal profit.’ To this day I don’t take any money for the picture. But David was an activist, and he wanted to get the word out there about how devastating AIDS was to families and communities. Honestly, I think he was a lot more in tune with how important these photos might become.”

Frare pauses, and laughs. “At the time, I was like, Besides, who’s going to see these pictures, anyway?

Over the past 20 years, by some estimates, as many as one billion people have seen the now-iconic Frare photograph that appeared in LIFE, as it was reproduced in hundreds of newspaper, magazine and TV stories — all over the world — focusing on the photo itself and (increasingly) on the controversies that surrounded it.

Frare’s photograph of David’s family comforting him in the hour of his death earned accolades, including a World Press Photo Award, when published in LIFE, but it became positively notorious two years later when Benetton used a colorized version of the photo in a provocative ad campaign. Individuals and groups ranging from Roman Catholics (who felt the picture mocked classical imagery of Mary cradling Christ after his crucifixion) to AIDS activists (furious at what they saw as corporate exploitation of death in order to sell T-shirts) voiced outrage. England’s high-profile AIDS charity, the Terrence Higgins Trust, called for a ban of the ad, labeling it offensive and unethical, while powerhouse fashion magazines like Elle, Vogue and Marie Claire refused to run it. Calling for a boycott of Benetton, London’s Sunday Times argued that “the only way to stop this madness is to vote with our cash.”

“We never had any reservations about allowing Benetton to use Therese’s photograph in that ad,” David Kirby’s mother, Kay, told LIFE.com. “What I objected to was everybody who put their two cents in about how outrageous they thought it was, when nobody knew anything about us, or about David. My son more or less starved to death at the end,” she said, bluntly, describing one of the grisly side effects of the disease. “We just felt it was time that people saw the truth about AIDS, and if Benetton could help in that effort, fine. That ad was the last chance for people to see David — a marker, to show that he was once here, among us.”

David Kirby passed away in April 1990, at the age of 32, not long after Frare began shooting at the hospice. But in an odd and ultimately revelatory twist, it turned out that she spent much more time with Peta, who himself was HIV-positive while caring for David, than she did with David himself. She gained renown for her devastating, compassionate picture of one young man dying of AIDS, but the photographs she made after David Kirby’s death revealed an even more complex and compelling tale.

Frare photographed Peta over the course of two years, until he, too, died of AIDS in the fall of 1992.

“Peta was an incredible person,” Frare says. Twenty years on, the affection in her voice is palpable. “He was dealing with all sorts of dualities in his life — he was half-Native American and half-White, a caregiver and a client at Pater Noster, a person who rode the line between genders, all of that — but he was also very, very strong.”

As Peta’s health deteriorated in early 1992 — as his HIV-positive status transitioned to AIDS — the Kirbys began to care for him, in much the same way that Peta had cared for their son in the final months of his life. Peta had comforted David; spoken to him; held him; tried to relieve his pain and loneliness through simple human contact — and the Kirbys resolved to do the same for Peta, to be there for him as his strength and his vitality faded.

Kay Kirby told LIFE.com that she “made up my mind when David was dying and Peta was helping to care for him, that when Peta’s time came — and we all knew it would come — that we would care for him. There was never any question. We were going to take care of Peta. That was that.

“For a while there,” Kay remembers, “I took care of Peta as often as I could. It was hard, because we couldn’t afford to be there all the time. But Bill would come in on weekends and we did the best we could in the short time we had.”

Kay describes Peta, as his condition worsened in late 1991 and 1992, as a “very difficult patient. He was very clear and vocal about what he wanted, and when he wanted it. But during all the time we cared for him, I can only recall once when he yelled at me. I yelled right back at him — he knew I was not going to let him get away with that sort of behavior — and we went on from there.”

Bill and Kay Kirby were, in effect, the house parents for the home where Peta spent his last months.

“My husband and I were hurt by the way David was treated in the small country hospital near our home where he spent time after coming back to Ohio,” Kay Kirby said. “Even the person who handed out menus refused to let David hold one [for fear of infection]. She would read out the meals to him from the doorway. We told ourselves that we would help other people with AIDS avoid all that, and we tried to make sure that Peta never went through it.”

“I had worked for newspapers for about 12 years already when I went to grad school,” Therese Frare says, “and was very interested in covering AIDS by the time I got to Columbus. Of course, it was difficult to find a community of people with HIV and AIDS willing to be photographed back then, but when I was given the okay to take pictures at Pater Noster I knew I was doing something that was important — important to me, at least. I never believed that it would lead to being published in LIFE, or winning awards, or being involved in anything controversial — certainly nothing as epic as the Benetton controversy. In the end, the picture of David became the one image that was seen around the world, but there was so much more that I had tried to document with Peta, and the Kirbys and the other people at Pater Noster. And all of that sort of got lost, and forgotten.”

Lost and forgotten — or, at the very least, utterly overshadowed — until LIFE.com contacted Frare, and asked her where the photo of David Kirby came from.

“You know, at the time the Benetton ad was running, and the controversy over their use of my picture of David was really raging, I was falling apart,” Frare says. “I was falling to pieces. But Bill Kirby told me something I never forgot. He said, ‘Listen, Therese. Benetton didn’t use us, or exploit us. We used them. Because of them, your photo was seen all over the world, and that’s exactly what David wanted.’ And I just held on to that.”

After the Benetton controversy finally subsided, Therese Frare went on to other work, other photography, freelancing from Seattle for the New YorkTimes, major magazines and other outlets. While the world has become more familiar with HIV and AIDS in the intervening years, Frare’s photograph went a long way toward dispelling some of the fear and, at times, willful ignorance that had accompanied any mention of the disease. Barb Cordle, volunteer director at Pater Noster when David Kirby was there, once said that Frare’s famous photo “has done more to soften people’s hearts on AIDS than any other I have ever seen. You can’t look at that picture and hate a person with AIDS. You just can’t.”

Life expectancy for people with HIV approaching that of general population.

A new study suggests the life expectancy of Canadians and Americans who are HIV positive is closing in on that of the general population.

The study says that a 20-year old diagnosed with HIV today can expect to live into their early 70s.

A couple of decades ago, a diagnosis of HIV was a death sentence for most who received it.

But with the discovery and improvement of antiretroviral drugs, HIV has become a chronic disease for most who have access to and can afford the medication.

A leading HIV researcher, Dr. Julio Montaner, says the findings of the study are excellent news.

Montaner is director of the B.C. Centre for Excellence in HIV/AIDS, which led the research collaboration that produced the study, which is published in the journal PLoS One.

He says the longevity gains have been remarkable. In 2000, a 20-year-old newly diagnosed with HIV could expect to live another 36 years. By 2006, that figure had climbed to 51 years.

“I don’t think, in all honesty, that there has been an area of medicine that has undergone a revolutionary evolution over our lifetime as HIV has,” Montaner says.

Dr. Ann Stewart, medical director of Toronto’s Casey House, agrees.

Casey House started 25 years ago as a hospice for dying AIDS patients. As treatment has prolonged the lives of the community it serves, the facility has transitioned into a hospital that offers care for people living with HIV.

Stewart says the findings of the study mirror what Casey House staff see in their patient population. But she warned that the picture is not an “unclouded” one — HIV-positive people often develop the health problems of age faster than those who are not infected.

So heart problems, cancers and the onset of dementia that might be expected in the late 60s, 70s or even 80s in HIV-negative people can show up in the 50s for HIV-positive people, she says.

“It’s much better than it was, for sure. For sure. But it’s not without challenges,” Stewart says.

“You can have HIV and live a wonderful life. But there’s certain complications and challenges associated with it as there are with other chronic diseases that you’re going to struggle with. So it’s not an unclouded sky.”

Cell-suicide blocker holds promise as HIV therapy.

NIBSC/Science Photo Library

Immune cells (green) infected with HIV (pink) undergo a cell-suicide process known as pyroptosis.

HIV infection causes a mass suicide of immune cells — a process that can be halted by an experimental drug that blocks cellular self-destruction, studies in cell cultures suggest. Researchers are now proposing a clinical trial of the drug in people with HIV.

Current HIV therapies act by targeting key proteins made by the virus. But findings from cell cultures, published today in Science1 and Nature2, suggest that targeting proteins in host cells might be an alternative approach to preserving the immune system in the face of an HIV infection.

The papers also address a decades-old mystery: why infection-fighting immune cells die off in people with HIV. A 2010 study3 showed that HIV does not directly kill most of these cells, called CD4 cells. Instead, the cells often self-destruct. “It’s much more a suicide than it is a murder,” says Warner Greene, a molecular virologist at the Gladstone Institute of Virology and Immunology in San Francisco, California, and a co-author of both the latest works.

Ring of fire

In the latest studies, Greene’s team investigated these ‘abortive’ infections. They identified a sensor that detects viral DNA in the cell and activates the suicide response1. And they found that most of the cellular suicide occurs via a process called pyroptosis, in which the dying cells unleash a ferocious inflammatory response2. A key protein involved in pyroptosis is caspase 1, and an experimental caspase-1 inhibitor made by Vertex Pharmaceuticals in Cambridge, Massachusetts, had already been tested in humans as a potential treatment for epilepsy. The drug, VX-765, failed to help epileptics, but six-week-long studies suggested that it was safe.

Greene and his colleagues tested VX-765 in HIV-infected cells cultured from human tonsils and spleens, and found that it blocked pyroptosis, prevented CD4 cell death, and suppressed inflammation. Greene hopes that the approach could one day provide an alternative or embellishment to the antiretroviral drugs currently used by 9.7 million people worldwide to manage HIV infection.

Because a caspase-1 inhibitor would target a host protein rather than the virus, HIV is less likely to become resistant to the therapy, says Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases in Bethesda, Maryland. But any new HIV therapy will face steep competition from the more than 30 antiretroviral drugs currently available. “You’ve got to be pretty good to replace the antiretrovirals,” says Fauci.


Understanding why HIV infection kills CD4 cells is an important step for researchers, says Gary Nabel, chief scientific officer at Sanofi, a pharmaceutical company headquartered in Paris. “We need to understand when a cell would rather die than let a virus infect it, and how the virus can evade that cellular suicide response to infection,” he says.

But Nabel also urges caution. He worries that some of the infections that Greene and his team consider abortive may progress if the immune cells survive. “Preventing cell death is a double-edged sword in the context of HIV,” he says. “Death can be protective if a T cell says ‘I’m going to die before I let this virus replicate and spread to other cells.’”

Greene counters that his team looked for evidence of progression to active infection, and found none. “Pyroptosis is not a strategy to protect the host from productive infection,” says Greene. “Instead, this is a pathway that actually promotes clinical progression to AIDS.”

New Dangerous Strain Of HIV Discovered

Researchers have discovered a new, more aggressive strain of the human immunodeficiency virus (HIV) that develops into AIDS much more quickly than other strains, Medical News Today reported.

In a new study published in the Journal of Infectious Diseases, scientists detailed the new strain as a “recombinant” virus – a hybrid of two virus strains. Called A3/02 – a cross between the 02AG and A3 viruses – the strain can develop into AIDS in just five years after first infection – one of the shortest time periods for HIV-1 types.

“Recombinants seem to be more vigorous and more aggressive than the strains from which they developed,” said first author Angelica Palm, a doctoral candidate at Lund University in Sweden.

So far, the A3/02 strain has only been seen in Guinea-Bissau, West Africa, but other studies have shown that recombinants are spreading more quickly across the globe.

“HIV is an extremely dynamic and variable virus. New subtypes and recombinant forms of HIV-1 have been introduced to our part of the world, and it is highly likely that there are a large number of circulating recombinants of which we know little or nothing,” said senior author Patrik Medstran, professor of clinical virology at Lund University. “We therefore need to be aware of how the HIV-1 epidemic changes over time.”

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Obama Launches HIV Cure Initiative, Ups Pledge For Global Health.


President Obama walks into an auditorium in the Eisenhower Executive Office Building Monday for a speech about World AIDS Day.

President Obama walks into an auditorium in the Eisenhower Executive Office Building Monday for a speech about World AIDS Day.

Carolyn Kaster/AP


Commemorating the 25th World AIDS Day a day late, President Obama announced an initiative Monday to find a cure for HIV infections that would be funded by $100 million shifted from existing spending.


“The United States should be at the forefront of new discoveries into how to put people into long-term remission without requiring lifelong therapies — or better yet, eliminate it completely,” Obama said at a meeting in the Eisenhower Executive Office Building next to the White House.


The initiative reflects a growing optimism among scientists that it may be possible to get patients’ immune systems to control HIV without drugs, or even to eliminate the virus from their systems. A feat like that seemed impossible not so long ago. The moneywill come from expiring AIDS research grants over the next three years, the administration said in a statement.


The president also pledged $5 billion over the next three years to the Global Fund to Fight AIDS, TB and Malaria if other countries contribute twice that amount. The Global Fund is holding its fourth replenishment meeting this week in Washington, with a goal of topping the $9.3 billion pledged three years ago.


And he signed legislation enacted last month to extend the 10-year-old President’s Emergency Program for AIDS Relief, or PEPFAR, started by President Bush.


Obama boasted that PEPFAR has exceeded the goal — thought to be ambitious when he set it on World AIDS Day two years ago – of getting anti-HIV treatment to 6 million people in developing countries. “Today I’m proud to announce that we’ve not only reached our goal, we’ve exceeded our treatment goal,” he said. “We’ve helped 6.7 million people receive life-saving treatment, and we’re going to keep at it.”


Obama also noted that the waiting list for treatment under the federal-state AIDS Drug Assistance Program last week fell to zero, from a peak of 9,310 in the fall of 2011.


Apart from that domestic bright spot, however, a report card on how America is doing with its own HIV epidemic reveals only slow progress.


In a panel discussion following Obama’s remarks, Dr. Chris Beyrer of Johns Hopkins University pointed out that when PEPFAR and the Global Fund began, AIDS experts were betting it would be easier to combat HIV in targeted populations in America than to get millions of HIV-infected people in sub-Saharan Africa into treatment.


But the opposite has happened. “African-American men are about half as likely” to have their HIV infection under control as non-Hispanic white men, Beyrer says. “And two-thirds of new infections are among men who have sex with men.”


The White House report is thin on promising results, as one section puts it, and heavy on challenges.


For instance, a 2010 National AIDS Strategy set a goal of reducing new HIV infections in this country by 25 percent. But the incidence “remains unacceptably high,” the latest report says. And, in fact, new HIV infections increased 12 percent among men who have sex with men in the most recent figures – 22 percent among the youngest males, from 13 to 24 years old.


The strategy aimed to increase the percent of HIV-infected who know their status to 90 percent. But the most recent figures indicate undiagnosed HIV decreased by only 9 percent between 2006 and 2010. And fewer than half of those between ages 13 and 24 years are aware of their infection.


When it comes to effective anti-HIV treatment, fewer than half of Americans at highest risk – men who have sex with men, blacks and Latinos – get sufficient antivirals drugs to keep their HIV under control.


Still, there’s evidence that concerted efforts to combat HIV can pay off in the most heavily affected places. The report cites impressive gains in New York City, the District of Columbia and San Francisco.


“All three have made care and treatment very available, have ramped up testing and needle exchanges,” says Chris Collins, policy director of amfAR, the American Foundation for AIDS Research. “When you do that, you see infection rates fall.”


For instance, when Washington, D.C., increased publicly funded HIV testing from 400 tests in 2007 to 120,000 in 2011, newly diagnosed cases went down by almost half. Newly diagnosed cases have also fallen by half in New York City and San Francisco.


The proportion of HIV-treated people whose virus was suppressed has gone steadily up in New York City, especially after the health department recommended that all newly diagnosed patients should be offered anti-retroviral treatment. By the end of last year, nearly 8 in 10 were virally suppressed.


Wayne C. Koff describes a scientific project that promises to accelerate the development of next-generation weapons in the fight against deadly infectious diseases.

Vaccines are one of the great success stories in the history of individual and public health. They have helped rid the planet of the scourge of smallpox, are poised to eliminate polio, and each year prevent millions of deaths, reducing the suffering and costs caused by infectious diseases.

But there are still many diseases for which vaccines do not yet exist. Moreover, strategies that have previously led to the successful development of vaccines are unlikely to work against more complex bacteria or viruses, such as HIV, which have evolved multiple mechanisms to evade the immune system.

The history of vaccinology is one in which biomedical and technological advances usher in the “next generation” of vaccines. In the 1950’s, a breakthrough that enabled viruses to grow in tissue cultures led to the development of both live attenuated vaccines and inactivated vaccines for measles, polio, and other diseases. In the 1980’s, recombinant DNA technology led to the development of vaccines against hepatitis B and human papillomavirus.

Around the turn of the century, the first sequencing of the human genome led to “reverse vaccinology.” This approach, whereby computational analysis of a pathogen’s genome enables identification and screening of a great many more potential vaccine targets than was previously possible, was used in the successful development of a vaccine against meningitis B.

The past decade has already yielded major advances in structure-assisted vaccine discovery, synthetic biology, systems biology, and immune monitoring. However, successfully translating these advances into the development of next-generation vaccines continues to be impeded by gaps in our understanding of the human immune response that protects against specific bacteria, viruses, or parasites.

That is why I, along with eight fellow scientists, have proposed the establishment of a new human-immunology-based clinical-research initiative, the Human Vaccines Project. In February 2014, leading scientists and public-health specialists will gather in La Jolla, California, to craft a scientific plan to identify, prioritize, and, most important, solve the major problems currently hindering development of vaccines against diseases such as AIDS, tuberculosis, and malaria.

Such a project would represent a paradigm shift in vaccine development. The current process is long (often spanning decades from concept to licensure), has a low probability of success (because of the limitations of animal models in predicting immune response and efficacy in humans), and is costly (often requiring hundreds of millions of dollars to develop a single vaccine).

Consider this: In just the past few years, many candidate vaccines against HIV, dengue, herpes, tuberculosis, and staphylococcus aureus have failed, at a cost of more than $1 billion. Investing that amount over the next decade in a coordinated effort to address the major questions facing vaccine development would rapidly accelerate our search for effective solutions, implying a transformative impact on individual and public health.

HIV presents perhaps the greatest challenge, because the virus leverages its extensive genetic variability to hide from the immune system. Using recent advances, however, scientists have now identified highly conserved regions of this variable virus, determined their molecular structure, and begun designing next-generation vaccine candidates to elicit antibodies that target these regions to prevent HIV infection. But HIV vaccine development, like that for several other diseases, is still impeded by the limitations of what animal models can tell us about how to elicit the necessary immune responses in humans.

Two recent advances could accelerate vaccine development and reduce its costs dramatically. In synthetic biology, the rapid engineering of nucleic acid-based vaccines means more candidates move more quickly from concept to trial. In systems biology, high-throughput technologies have increased the number of genetic and immunologic parameters assessed in trials. This approach has helped predict the efficacy of potential new-generation vaccines against yellow fever and influenza within days of immunization, compared with the usual timeframe of months or years.

Vaccines already prevent the deaths of 2-3 million people every year, preempt human suffering, lighten the burden placed on health-care systems, and enable more rapid economic and social development. Models show that adding even a partly effective AIDS vaccine to the current range of prevention and treatment procedures could dramatically lower the rate of HIV infection.

As the Nobel Peace Prize laureate Desmond Tutu, one of the world’s great campaigners against HIV/AIDS, wrote recently: “We must make the most of scientific advances over the last half-century, which have made vaccines for other preventable diseases the most powerful and cost-effective health-care investment that currently exists.”

That is the idea behind the Human Vaccines Project – a concept that would have been unimaginable even a decade ago. Today, technological advances in vaccine discovery and immune monitoring allow us realistically to explore this potentially game-changing approach to disease prevention. February’s gathering in California may take us a giant step closer to a world without deadly and debilitating infectious diseases.

World Aids Day 2013: The war on the epidemic is being won, but discrimination … – The Independent

The battle against Aids is being won, with deaths down, record numbers of people being treated, and new cases among children down by more than half.

Deaths are down, however battling the stigma is the main obstacle to beating HIV once and for all

But ongoing discrimination against sufferers is the biggest obstacle to winning the war, according to the head of the United Nations Joint Programme on HIV/Aids (UNAIDS).

Speaking to The Independent on Sunday on the eve of World Aids Day, UNAIDS executive director Michel Sidibé said: “We are winning against this epidemic, we are seeing a decline in new infections, an increase in people treated… we have broken the conspiracy of silence.”

For the first time, he said, authorities can see “an end to an epidemic that has wrought such staggering devastation around the world”.

He added: “People living with HIV can live long and healthy lives, can now protect their partners from becoming infected, and can keep their children free from HIV.”

But Mr Sidibé also warned: “We have not been able to change completely the perception of people against the most-at-risk populations. The stigma, discrimination and criminalisation of those people – sex workers, people who inject drugs, men who have sex with men – all those groups are mainly at risk of continuing to be completely forgotten.”

There are more than 70 countries with “homophobic laws” – something which demonstrates “we still have a long way to go”.

Discrimination remains a major obstacle in many parts of the world. One in seven people living with HIV has been denied access to healthcare and more than one in 10 has been refused employment. And while the global picture is good, austerity-stricken Europe is at risk of repeated outbreaks of HIV, warned the World Health Organization last night.

In a bid to end the persecution of people with HIV/Aids, UNAIDS is launching a “zero discrimination” campaign, backed by Nobel Peace Prize Winner Daw Aung San Suu Kyi, to mark World Aids Day.

Speaking at today’s launch of the campaign to launch a Zero Discrimination Day on 1 March 2014, she said: “We can all make a difference by reaching out and letting people lead a life of dignity, irrespective of who they are.”

North America and Caribbean

Aids-related deaths in the Caribbean dropped 50 per cent between 2001 and 2012 (falling from 24,000 to 11,000), but in Jamaica 37 per cent of gay men are HIV positive. Mexico has an HIV rate among gay men of 17 per cent; Guyana 19 per cent. Meanwhile, 17 per cent of Guyanese sex workers are HIV positive, against 1 per cent in Mexico.

South America

Across Latin America there was a 37 per cent drop in Aids deaths between 2001 and 2012 – from 82,000 to 52,000. With its high deprivation and population density, Brazil’s HIV rate is among the highest; 10 per cent of gay men, and 5 per cent of sex workers, are HIV positive. In Peru, where less than 0.4 per cent of the population is HIV positive, 12 per cent of gay men are infected.


In sub-Saharan countries the number of new cases of HIV was 40 per cent less last year than in 2001 – almost a million fewer cases. But with some 1.6 million people infected last year, the continent’s struggle with Aids and HIV continues. In Swaziland, one in four adults (26 per cent) is HIV positive. Across the continent there were 1.2 million Aids-related deaths last year. The majority of those infected with HIV were sex workers and gay men. In Ivory Coast half of “men who sleep with men” are HIV positive. By contrast, in developed Middle East and North Africa, numbers acquiring HIV rose by more than 50 per cent, but still remained at just 32,000 people in 2012.

Europe and Central Asia

HIV infections have increased by 13 per cent, or 100,000 people, since 2006. The majority of people diagnosed with HIV were those who inject drugs, and gay men. Across the continent, less than 1 per cent of the population was HIV positive. The Ukraine, Belarus and Spain had the highest HIV rates among needle users, with 21, 17 and 16 per cent respectively. The number of Aids-related deaths in the region has increased from 36,000 in 2001 to 91,000 people last year. New infections among drug users in Greece have risen, despite a general decline elsewhere in Europe, with authorities blaming funding cuts in treatment centres.

East and South-east Asia

Aids deaths were on the rise in East Asia last year, increasing from 18,000 in 2001 to 41,000. A fifth of Thailand’s gay men and needle users were HIV positive, compared with 0.6 per cent of the general population. In the Philippines only 1 per cent of gay men had been infected, but 14 per cent of drug users were positive. In Indonesia 9 per cent of sex workers were HIV positive.

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