News (Updated July 22, 2007)
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SYDNEY, July 19, 2007 (AFP) - A new generation of HIV drugs is so promising that researchers are talking about eradicating the virus, an international AIDS conference will be told in Sydney next week.
The International AIDS Society (IAS) conference from July 22-25 will bring together more than 5,000 experts from around the world to hear presentations on the cutting edge of HIV/AIDS research.
Conference co-chairman David Cooper said the research ranged from studies showing a simple measure such as male circumcision can reduce the risk of HIV infection by up to 60 percent to details of the latest hi-tech pharmaceuticals.
Cooper said some of the most exciting research developments came from a new generation of drugs called integrase inhibitors, which help block the HIV virus infecting new cells.
Cooper said while cocktails of powerful anti-retroviral drugs had been used to help contain the virus and prolong life for more than a decade, the new drugs were more potent than their predecessors and had fewer side effects.
Cooper, the director of Australia's National Centre for HIV Epidemiology and Clinical Research, said integrase inhibitors and other promising research avenues such as gene therapy meant eradicating HIV was a realistic possibility.
"The integrase inhibitors are particularly potent drugs and I think you will start to see that eradication will return to the agenda with these new agents and new ways of using them," Cooper told reporters.
"Eradication was talked about when anti-retroviral therapies became available in the mid-1990s but went off the agenda because of the toxicity of the drugs -- people thought it was going to take 50 years.
"Now with some of the newer drugs and newer strategies it's back on the agenda again."
Cooper said up to 30 drugs were now available to HIV patients in the developed world, meaning they live longer but present a challenge to the health systems which treat them because they are more prone to conditions such as heart disease and cancer.
He said a major topic for discussion at the conference was making the latest drugs available in impoverished developing countries.
"In the developing world, we've only got the standard older drugs, which are more toxic," he said.
"One of the tensions is how we get these really new medications into the developing world."
Anthony Fauci, the director of the US National Institute of Allergy and Infectious Diseases, said about two million people were being treated with anti-retroviral drugs in developing nations but the aim was quadruple that number.
Fauci said US President George W. Bush committed 30 billion dollars to HIV AIDS treatment in the developing world last May, in what amounted to the largest public health campaign ever undertaken.
"The achievements in treatment have been breathtaking, there has been so much accomplished in the years up to 2007, but there is still much to do -- that will be the key message I'll be taking to the conference," he told AFP.
To help ensure that anti-retroviral medicines are properly rolled out in countries which often lack basic infrastructure, Cooper has proposed delegates at the conference sign an initiative called the "Sydney Declaration."
The declaration will earmark 10 percent of HIV/AIDS funding in the developing world for research, to ensure programmes are working efficiently.
"If donors can't see that there's good outcomes, that it's effective, then unfortunately they're going to pull the plug," Cooper said. "The only way to keep it on track is with research."
WASHINGTON (Reuters) - Researchers have a new clue about why a widely used AIDS drug has certain side effects such as mysterious fat deposits, they reported on Monday.
Parallels between the side effects of protease inhibitors -- a critical component of HIV drug cocktails -- and genetic conditions that cause early aging may help explain the often debilitating fat deposits and other results, they said.
Protease inhibitors can cause metabolic problems such as an unhealthy buildup of cholesterol in the blood, high blood pressure, and increased risk of diabetes.
They also trigger a condition called lipodystrophy -- a strange redistribution of body fat that gives some patients wasted cheeks and limbs, and a so-called "buffalo hump" of fat on the back of the neck.
Doctors have long been mystified by how protease inhibitors and other HIV drugs cause such effects, which occur in tens of thousands of drug takers worldwide, said Dr. Charles Flexner at Johns Hopkins University School of Medicine, who was not involved in this study.
In an attempt to shed light on this, a group at the University of California Los Angeles and Purdue University in Indiana treated mouse and human cells with protease inhibitor, and found that they accumulated a particularly clumpy form of a protein called prelamin A.
The drug triggered this by blocking the action of another protein -- called ZMPSTE24 -- that converts prelamin A into its useful form, they reported in the Proceedings of the National Academy of Sciences.
Cells with lower levels of ZMPSTE24 to begin with were particularly affected by the protease inhibitor.
Purdue University's Christine Hrycyna, who worked on the study, said that blocking this protein might contribute to the metabolic side effects of protease inhibitors.
Patients with early aging syndromes, including Hutchinson-Gilford progeria, have symptoms that mimic the side effects, and the same protein is clumped in their cells, said Hrycyna. But how this might affect metabolism is not clear, she said.
"The side effects are probably due not to just one simple thing," Hrycyna said.
"I think this paper may provide new insights into possible mechanisms for some of the side effects of protease inhibitors," added Flexner.
The researchers also tested some of the other drugs that are commonly used in AIDS cocktails, known as highly active antiretroviral therapy or HAART.
But the other drugs did not cause the same protein accumulation, even though they can cause similar side effects in people, the researchers wrote.
"They are probably due to a combination of all these different drugs," Hrycyna added.
The researchers now want to see if their theory holds true in HIV patients, and if versions of protease inhibitors that do not block ZMPSTE24 as much might cause fewer side effects in these patients.
Thu Jul 19, 2:50 PM ET
Three gene variants in the DNA of 486 AIDS patients appear to play a role in containing and slowing the HIV virus, according to research published Thursday.
The researchers hope their finding will lead to a vaccine that would boost the protective effects of one or more of these genes, and help the body's own immune system overcome an infection.
One gene variant looks specially promising, the scientists said in a study to appear in the Friday edition of the journal Science.
"These results not only approximately double our understanding of the factors that influence variation amongst individuals in how they control HIV-1, but also point toward new mechanisms of control," said David Goldstein, of Duke's Institute for Genome Sciences and Policy at North Carolina's Duke University and chief author of the study.
The international team of geneticists worked for 18 months in carefully selecting patients and using the latest in genome-wide screening technology to discover the three genes.
The research found that some patients with specific gene variants in key immune system cells appear to be much better controlling the proliferation of the AIDS virus after infection.
"As we expand the number of patients in future studies conducted by CHAVI (Center for HIV/AIDS Vaccine Immunology) researchers, we aim to discover even more polymorphisms that could provide additional clues how some patients are better able to control the virus than others," Goldstein said.
"This should ultimately lead to novel targets for vaccines, the primary goal of CHAVI," a seven-year project launched in 2005 by the National Institute of Allergy and Infectious Diseases (NIH).
Two of the newly discovered gene variants were found in genes controlling the human leukocyte antigen (HLA) system, which plays a "major role" in the immune system by identifying foreign invaders and "tagging" them for destruction.
Two of the HLA genes, known as HLA-A and B, are turned off by the HIV virus when it enters the body, which keeps the immune system from recognizing the virus as foreign.
However, the HLA-C gene is apparently not turned off by the AIDS virus, suggesting that for some individuals at least HLA-C is involved in controlling the HIV virus, the researchers said.
The HLA-C gene may represent an Achilles heel of HIV, according to Goldstein.
A vaccine could be designed to elicit an HLA-C mediated response that the HIV virus might be unable to defuse, the expert added.
Thu Jul 19, 5:19 AM ET
Scientific studies have confirmed a long-standing belief that male circumcision can reduce HIV infection rates in men by 60 percent, an international AIDS conference will be told next week.
David Cooper, the co-chairman of an International AIDS Society (IAS) conference to be held in Sydney from July 22-25, said research on male circumcision represented a major development in HIV prevention.
"We always knew that if you went into any particular African country that HIV rates among Muslim men were lots lower," Cooper told AFP.
"But we were never sure that the Muslim men had lower numbers of partners than non-Muslim men, so people always doubted it."
Cooper said the only way to ensure the link between lower HIV rates and circumcision was not due to cultural factors was to carry out random trials, the results of which will be presented at the Sydney conference.
He said three trials were conducted in South Africa, Kenya and Uganda, each involving more than 2,000 heterosexual men, half of whom were circumcised.
"The reduction in HIV infection was about 60 percent, so clearly it works," said Cooper, who is also the director of Australia's National Centre for HIV Epidemiology and Clinical Research.
Cooper said the studies showed circumcision could be a powerful tool in helping curb HIV infection in sub-Saharan Africa, where infection rates in some countries are up to 40 percent of the adult population.
He said, however, that any introduction of widespread male circumcision in developing countries needed to be carried out with an education campaign that reinforced a safe sex message.
"In some areas of sub-Saharan Africa men are requesting circumcision, which is a bit of a worry, as they may think they're protected and they're not," Cooper said.
"It merely reduces the risk, you still have to use condoms, men can't think 'that's all I need to do, I can now have unsafe sex'."
The clinical reason for circumcision's preventive effect is still being investigated.
One theory is that the foreskin has a very thin lining and suffers minor abrasions during intercourse, making it easier for the human immunodeficiency virus (HIV) to enter the man's bloodstream. Another is that the foreskin is rich in Langerhans cells, whose surface is configured in such a way that the AIDS virus readily latches on to them.
Wed Jul 18, 7:08 PM ET
Patients who successfully respond to drugs that combat the AIDS virus can see a key marker of immune health rebound to a level enjoyed by people without HIV, a study published online Wednesday by The Lancet says.
The paper sheds light on poorly understood conditions as to why some people on antiretroviral drugs can boost and maintain their CD4 immune cells, others see a slower increase in these key defenders while other individuals fail, sometimes tragically so.
Investigators led by Amanda Mocroft of London's Royal Free Centre for HIV Medicine looked at 1,835 people with the human immunodeficiency virus (HIV) before and after they were put on antiretrovirals.
On average, these individuals had a CD4 count of 204 cells per microlitre of blood at the start of the study.
In the first year of taking antiretrovirals, there was a big spurt in the CD4 count, of around 100 cells per microlitre on average.
HIV levels were also suppressed, to below 50 copies of the virus per microlitre, which is considered a key goal in antiretroviral treatment.
Over the next few years, lower -- but still significant -- improvements in the CD4 count continued.
In fact, after three years, patients who had started therapy with a CD4 count of more than 350 cells per microlitre had a CD4 count "approaching the level seen in HIV-negative individuals," Mocroft says.
On average, the boost was around 50 cells per microlitre annually, and this continued even up to the fifth year of treatment, which by the standards of HIV therapy is a long time indeed.
Most rewarding of all was that this enduring improvement was seen among patients who had had low CD4 cells (of less than 200 cells per microlitre) before they began therapy.
Those who began with more than 500 CD4 cells per microlitre saw the least relative improvement.
The upturn in CD4 cells only occurs, though, if patients continue to respond well to the drugs and can keep their HIV count to below 50 copies per microlitre, the authors warn.
CD4 cells are frontline guardians of the immune system and their levels are closely watched barometers of a patient's ability to fight off opportunistic disease and death.
Previous research in this field has been more pessimistic, suggesting that CD4 counts tend to plateau after several years of treatment.
But those studies used less strict criteria for determining whether the drugs were working.
Their benchmark was a viral load -- the number of AIDS viruses in the blood -- of 1,000 and 400 copies per microlitre, whereas the new study sets a far tougher standard of 50 copies or less.
The paper is published by The Lancet ahead of a meeting in Sydney from Sunday to July 25 of the International AIDS Society, which will focus especially on HIV treatment.
Friday July 20, 1:16 pm ET
The drug candidate, SP-01A, is being studied as both a monotherapy and an adjunctive, or combination, therapy. The Phase IIb study compared the drug with placebo and involved 43 patients in three dosing groups. The company said it and its partner Pharmaplaz plan to submit final study data to the Food and Drug Administration and the European Medicines Agency.
Thursday July 19, 4:38 pm ET
The company earned $407.9 million, or 42 cents per share, compared with profit of $265.2 million, or 28 cents per share, during the same period last year.
Revenue surged 53 percent to $1.05 billion from $685.3 million.
Analysts polled by Thomson Financial expected profit of 39 cents per share on revenue of $1.02 billion.
Sales of Atripla rose 12 percent to $212.4 million. The drug is a once-a-day HIV treatment combining Gilead's Truvada -- which includes Viread and Emtriva -- and Bristol-Myers Squibb's Sustiva. Sales of Truvada jumped 29 percent to $385.4 million, while sales of Viread fell 7 percent to $154.9 million.
Other positive news included a 32 percent rise in sales to $75.2 million for hepatitis B drug Hepsera.
Thursday July 19, 6:17 pm ET
Pfizer is seeking marketing approval for Celsentri from European regulators, who will weigh the opinion of the Committee for Medicinal Products for Human Use when they make a final decision in coming months.
Unlike most HIV treatments currently available, Celsentri does not attack HIV directly, but instead blocks the virus from entering cells in the first place. If approved the drug would mainly be used by patients who have stopped responding to conventional HIV treatments.
In April, U.S. health advisers recommended the Food and Drug Administration approve the drug, also known as maraviroc. But last month the agency stopped short of making a decision and asked Pfizer for more information about the drug.