News (Updated December 17, 2010)

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German doctors declare "cure" in HIV patient

Dec 15, 2010

By Maggie Fox, Health and Science Editor

WASHINGTON (Reuters) - German researchers who used a bone marrow transplant to treat a cancer patient with the AIDS virus, have declared him cured of the virus -- a stunning claim in a field where the word "cure" is barely whispered.

The patient, who had both HIV infection and leukemia, received the bone marrow transplant in 2007 from a donor who had a genetic mutation known to give patients a natural immunity to the virus.

Nearly four years after the transplant, the patient is free of the virus and it does not appear to be hiding anywhere in his body, Thomas Schneider of Berlin Charite hospital and colleagues said.

"Our results strongly suggest that cure of HIV has been achieved in this patient," they wrote in the journal Blood.

AIDS researchers have rejected the approach on any kind of scale for patients with HIV. A bone marrow transplant is a last-ditch treatment for cancers such as leukemia.

It requires destruction of a patient's own bone marrow -- itself a harrowing process -- and then a transplant from a donor who has a near-exact blood and immune system type. Months of recovery are needed while the transplant grows and reconstitutes the patient's immune system.

"It's not practical and it can kill people," said Dr. Robert Gallo of the Institute of Human Virology at the University of Maryland , who helped discover the human immunodeficiency virus that causes AIDS.

"It is possibly a cure, that's for sure, you won't know for absolute sure until the person dies and undergoes extreme PCR (genetic) analysis of post-mortem tissue."

The mutation affects a receptor, a cellular doorway, called CCR5, that the AIDS virus uses to get into the cells it infects.

Since the 1990s scientists have known that some people, mostly of Northern European descent, have the mutation and are rarely infected with HIV.

"They are uninfectable, virtually," Gallo said.

Some researchers are working on the idea of gene therapy to treat or try to cure HIV, but the technology is still in experimental stages.

"I don't want to throw cold water on an interesting thing, but that's what it is -- an interesting thing," Gallo said.

Schneider's team has been following the patient, taking samples from his colon, liver, spinal fluid and brain as he developed various conditions that justified the tests. They tested all these samples for evidence of the virus, which can be difficult to detect unless it is actively infecting cells.

All these places are suspected "reservoirs" where HIV can hide out for years, to rebound in patients who stop taking drugs that suppress the infection.

This patient appears to have a fully functioning immune system, they found, which appears genetically identical to cells from the donor -- not the patient's own immune cells.

Schneider's team found no evidence of HIV anywhere.

"From these results, it is reasonable to conclude that cure of HIV infection has been achieved in this patient," they wrote.

The AIDS virus infects 33 million people globally and has killed more than 25 million since the pandemic began in the 1980s. Cocktails of strong drugs can suppress the virus, keeping patients healthy and reducing the chance they will infect others, but there is no vaccine.

(Editing by Chris Wilson)

Britain is tuberculosis capital of Europe

Dec 17 2010

By Kate Kelland

LONDON (Reuters) - Britain is the only country in Western Europe with rising rates of tuberculosis and in London cases of the disease once dubbed "the white plague" have grown by nearly 50 percent since 1999, a study showed on Friday.

Britain has more than 9,000 cases of tuberculosis (TB) diagnosed a year and the problem is becoming particularly acute in the capital, which accounts for 40 percent of the nation's total diagnosed cases, researchers said.

Alimuddin Zumla, a global TB expert from University College London, said the situation in London was reminiscent of outbreaks of multi-drug resistant TB in prisons in the United States in the 1990s -- outbreaks that required a large financial investment to be brought under control.

TB -- referred to as the "white plague" during Victorian times because sufferers' skin tone turned so pale -- could come back with a vengeance in poverty-stricken areas.

"Poor housing, inadequate ventilation, and overcrowding -- conditions prevalent in Victorian Britain -- are causes of the higher TB incidence rates in certain London boroughs," he said in a commentary on the study, which was published in the Lancet Infectious Diseases journal.

He said that in Britain , as in all European countries, the disease was mainly concentrated in high-risk groups such as migrants, refugees, homeless people, drug users, prisoners, and people infected with the HIV virus that causes AIDS.

A report last month found that cases of tuberculosis in Britain reached their highest level for 30 years in 2009 with 9,040 cases, and the number of new drug-resistant TB cases had almost doubled in the past decade.

Up to a third of people worldwide are infected with the bacterium that causes TB, although only a small percentage ever develop the disease. Studies show that people with substance abuse problems and those who live in hard-to-reach communities are more prone to the illness than the general population.

The AIDS epidemic drove up the number of TB cases across the world in the late 1980s and 1990s because the immune suppression caused by HIV can make a person far more susceptible to TB.

People can get drug-resistant forms of the TB either as a result of catching such a strain from another person or because of inappropriate or incomplete treatment.

This study found that the increase in the number of TB cases seen in Britain has largely been in non-UK born groups, but most of these were not in new migrants. It said 85 percent of cases born overseas had lived in Britain for two or more years and about half had lived here for five or more years -- indicating that the disease is not being imported from elsewhere.

(Editing by Alison Williams)

Primate Immune System Differences Identified

Research may also help explain why chimpanzees don't routinely develop AIDS after HIV exposure

Dec. 17, 2010 (HealthDay News) -- Differences in immune signaling pathways among various species may explain why humans are more susceptible than other primates to certain infectious diseases, researchers say.

For example, when it comes to the progression of HIV to AIDS or severe complications from hepatitis B, it has been found that humans are more sensitive than chimpanzees to the serious effects of these viral infections, noted Luis B. Barreiro of the University of Chicago and colleagues.

In the new study, published in the Dec. 16 online edition of the journal PLoS Genetics, Barreiro 's team conducted the first genome-wide comparison of genes regulated by the innate immune system in humans, chimpanzees and rhesus macaques. In order to identify functional differences in their immune pathways, the researchers stimulated immune cells from each of the three primate species.

The core response needed to fight any invading pathogen was similar in all three species. But there were differences in how the immune system fought off certain viral and microbial infections. This likely reflects rapid adaptation cycles between specific hosts and viruses, the study authors said.

One particularly interesting finding was that many HIV-interacting genes responded uniquely in chimpanzees, which may help explain why chimpanzees do not routinely develop AIDS after being infected with HIV, the study authors noted in a news release from the journal's publisher.

The researchers also found that human immune responses were particularly enriched for genes involved in cell death and cancer biology.

How 'chameleon-like' HIV virus eludes treatment by mutating

2010-12-19

A new study has shed light on how chameleon-like HIV virus constantly mutates into forms and gets away even from the best cocktail of current therapies.

This understanding may help developing better tests and treatments for patients.

Stefan Sarafianos, of the University of Missouri , revealed that the discoveries provide clues into HIV's mechanisms for resisting two main families of drugs.

"These findings are important because identifying a new mutation that affects HIV drug resistance allows physicians to make better decisions and prescribe the proper drugs. Without that knowledge, therapy can be suboptimal and lead to early failure," said Sarafianos.

Patients with HIV are routinely tested to track the levels of the virus and immune cells in their body. Results of the tests help physicians gauge the health of their patients and prescribe the right mix of antiviral drugs.

The drugs help prevent the spread of HIV in patients by inhibiting the virus' ability to replicate.

Sarafianos' lab determined the biochemical properties that allow strains of HIV with a specific mutation-the N348I mutation-to escape inhibition despite treatment with Nevirapine.

Sarafianos' recent findings resulted from research supported by five National Institutes of Health grants.

The findings were published in the Journal of Biological Chemistry and Nature Structural and Molecular Biology. (ANI)

FDA Approves Once-Daily Darunavir for Certain Patients With HIV

Yael Waknine

December 15, 2010 — The US Food and Drug Administration (FDA) has approved once-daily dosing for darunavir (Prezista; Tibotec Pharmaceuticals, a division of Centocor Ortho Biotech Products, LP) boosted with ritonavir in treatment-experienced adult patients with HIV with no resistance to the protease inhibitor. Use of the darunavir/ritonavir 800 mg/100 mg once-daily regimen previously was restricted to treatment-naive patients.

"With this once-daily dosing recommendation, boosted Prezista is now a viable option for more treatment-experienced patients," said Glenn Mattes, president of Tibotec Therapeutics, in a company news release.

The new recommendation was based on 48-week data from the phase 3b Once-daily Darunavir In treatment-experieNced patients (ODIN) study of 590 patients with no darunavir resistance–associated mutations (V11I, V32I, L33F, I47V, I50V, I54M, I54L, T74P, L76V, I84V, or L89V), a screening viral load of more than 1000 HIV-1 RNA copies/mL, and a CD4+ count higher than 50 cells/mm3.

Patients had been on highly active antiretroviral therapy for at least 12 weeks and were randomly assigned to receive darunavir once or twice daily with food and an optimized background regimen of 2 or more nucleoside reverse transcriptase inhibitors selected by investigators.

Results showed that darunavir/ritonavir 800 mg/100 mg once daily was similarly effective to the 600 mg/100 mg twice-daily regimen for achieving virologic response, defined as HIV-1 RNA levels lower than 50 copies/mL (69% for both). The mean increase from baseline in CD4+ cell count was likewise comparable between treatment groups (108 cells/mm3 vs 112 cells/mm3).

The FDA notes that patients with 1 or more darunavir resistance–associated mutation, and those for whom genotypic testing is not feasible, must continue taking darunavir/ritonavir 600 mg/100 mg twice daily.

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