Given a paragraph, generate a claim that is supported by the given paragraph. 1) The claim must contain information from within the paragraph. 2) A sentence within the paragraph can be used as a claim. 3) The claim should not have contradictions within the paragraph. 4) The claim should be at most one sentence long.

Input: Consider Input: A still image provided by KPIX TV and taken from the broadcaster's video footage shows Timothy Ray Brown during an interview at his home in San Francisco. Timothy Ray Brown, was a young HIV-positive American living and working in Berlin who had developed leukaemia and suffered a relapse after initial treatment. REUTERS/Courtesy KPIX TV/Handout Dramatic scientific advances since HIV was first discovered 30 years ago this week mean the virus is no longer a death sentence. Thanks to tests that detect HIV early, new antiretroviral AIDS drugs that can control the virus for decades, and a range of ways to stop it being spread, 33.3 million people around the world are learning to live with HIV. People like Vuyiseka Dubula, an HIV-positive AIDS activist and mother in Cape Town, South Africa, can expect relatively normal, full lives. “I’m not thinking about death at all,” she says. “I’m taking my treatment and I’m living my life.”   Nonetheless, on the 30th birthday of HIV, the global scientific community is setting out with renewed vigor to try to kill it. The drive is partly about science, and partly about money. Treating HIV patients with lifelong courses of sophisticated drugs is becoming unaffordable. Caring for HIV patients in developing countries alone already costs around $13 billion a year and that could treble over the next 20 years. In tough economic times, the need to find a cure has become even more urgent, says Francoise Barre Sinoussi, who won a Nobel prize for her work in identifying Human Immunodeficiency Virus (HIV). “We have to think about the long term, including a strategy to find a cure,” she says. “We have to keep on searching until we find one.”   The Berlin patient is proof they could. His case has injected new energy into a field where people for years believed talk of a cure was irresponsible. Timothy Ray Brown was living in Berlin when besides being HIV-positive, he had a relapse of leukemia. He was dying. In 2007, his doctor, Gero Huetter, made a radical suggestion: a bone marrow transplant using cells from a donor with a rare genetic mutation, known as CCR5 delta 32. Scientists had known for a few years that people with this gene mutation had proved resistant to HIV. “We really didn’t know when we started this project what would happen,” Huetter, an oncologist and haematologist who now works at the University of Heidelberg in southern Germany, told Reuters. The treatment could well have finished Brown off. Instead he remains the only human ever to be cured of AIDS. “He has no replicating virus and he isn’t taking any medication. And he will now probably never have any problems with HIV,” says Huetter. Brown has since moved to San Francisco. Most experts say it is inconceivable Brown’s treatment could be a way of curing all patients. The procedure was expensive, complex and risky. To do this in others, exact match donors would have to be found in the tiny proportion of people — most of them of northern European descent — who have the mutation that makes them resistant to the virus. Dr Robert Gallo, of the Institute of Virology at the University of Maryland, puts it bluntly. “It’s not practical and it can kill people,” he said last year. Sinoussi is more expansive. “It’s clearly unrealistic to think that this medically heavy, extremely costly, barely reproducible approach could be replicated and scaled-up ... but from a scientist’s point of view, it has shown at least that a cure is possible,” she says. The International AIDS Society will this month formally add the aim of finding a cure to its HIV strategy of prevention, treatment and care. A group of scientist-activists is also launching a global working group to draw up a scientific plan of attack and persuade governments and research institutions to commit more funds. Money is starting to flow. The U.S. National Institutes of Health is asking for proposals for an $8.5 million collaborative research grant to search for a cure, and the Foundation for AIDS Research, or amfAR, has just announced its first round of four grants to research groups “to develop strategies for eradicating HIV infection.”   Until recently, people in HIV and AIDS circles feared that to direct funds toward the search for a cure risked detracting from the fight to get HIV-positive people treated. Even today, only just over five million of the 12 million or so people who need the drugs actually get them. HIV first surfaced in 1981, when scientists at the U.S. Centers for Disease Control and Prevention discovered it was the cause of acquired immunodeficiency syndrome (AIDS). An article in the CDC’s Morbidity and Mortality Weekly Report of that June referred to “five young men, all active homosexuals” from Los Angeles as the first documented cases. “That was the summer of ‘81. For the world it was the beginning of the era of HIV/AIDS, even though we didn’t know it was HIV then,” says Anthony Fauci, director of the U.S. National Institute of Allergy and Infectious Diseases, who has made AIDS research his life’s work. In the subsequent three decades, the disease ignorantly branded “the gay plague” has become one of the most vicious pandemics in human history. Transmitted in semen, blood and breast milk, HIV has devastated poorer regions, particularly sub-Saharan Africa, where the vast majority of HIV-positive people live. As more tests and treatment have become available, the number of new infections has been falling. But for every two with HIV who get a chance to start on AIDS drugs, five more join the “newly infected” list. United Nations data show that despite an array of potential prevention measures — from male circumcision to sophisticated vaginal or anal microbicide gels — more than 7,100 new people catch the virus every day. Treatment costs per patient can range from around $150 a year in poor countries, where drugs are available as cheap generics, to more than $20,000 a year in the United States. The overall sums are huge. A recent study as part of a non-governmental campaign called AIDS2031 suggests that low and middle-income countries will need $35 billion a year to properly address the pandemic by 2031. That’s almost three times the current level of around $13 billion a year. Add in the costs of treatment in rich countries and experts estimate the costs of HIV 20 years from now will reach $50 to $60 billion a year. “It’s clear that we have to look at another possible way of managing of the epidemic beyond just treating everyone forever,” says Sharon Lewin, a leading HIV doctor and researcher from Monash University in Melbourne, Australia. In some ways, we have been here before. Early AIDS drugs such as AZT came to market in the late 1980s, but within a decade they were overtaken by powerful cocktail treatments known as HAART, or highly active antiretroviral treatment. HAART had a dramatic effect — rapidly driving the virus out of patients’ blood and prompting some to say a cure was just around the corner. But then scientists discovered HIV could lie low in pools or reservoirs of latent infection that even powerful drugs could not reach. Talk of a cure all but died out. “Scientifically we had no means to say we were on the way to finding a cure,” says Bertrand Audoin, executive director of the Geneva-based International AIDS Society. “Scientists ... don’t want to make any more false promises. They didn’t want to talk about a cure again because it really wasn’t anywhere on the horizon.”   The ultimate goal would allow patients to stop taking AIDS drugs, knocking a hole in a $12 billion-a-year market dominated by Californian drugmaker Gilead and the likes of Pfizer, GlaxoSmithKline and Merck. It’s unlikely to happen anytime soon, but Brown’s case has opened the door to new ideas. “What it proved was that if you make someone’s cells resistant to HIV...then all the last bits of HIV, that hang around for a long time in patients on treatment, did in fact decay and disappear,” says Lewin. Now scientists working on mimicking the effect of the Berlin patient’s transplant have had some success. One experimental technique uses gene therapy to take out certain cells, make them resistant to HIV and then put them back into patients in the hope they will survive and spread. At an HIV conference in Boston earlier this year, American researchers presented data on six patients who had large numbers of white blood cells known as CD4 cells removed, manipulated to knock out the existing CCR5 gene, and then replaced. “It works like scissors and cuts a piece of genetic information out of the DNA, and then closes the gap,” says Huetter. “Then every cell arising from this mother cell has this same mutation.”   Early results showed the mutated cells managed to survive inside the bodies of the patients at low levels, remaining present for more than three months in five. “This was a proof of concept,” says Lewin. Another potential avenue is a small group of patients known as “elite controllers”, who despite being infected with HIV are able to keep it under control simply with their own immune systems. Researchers hope these patients could one day be the clue to developing a successful HIV/AIDS vaccine or functional cure. Scientists are also exploring ways to “wake up” HIV cells and kill them. As discovered in the late 1990s, HIV has a way of getting deep into the immune system itself — into what are known as resting memory T-cells — and going to sleep there. Hidden away, it effectively avoids drugs and the body’s own immune response. “Once it goes to sleep in a cell it can stay there forever, which is really the main reason why we can’t cure HIV with current drugs,” says Lewin. Her team in Melbourne and another group in the United States are about to start the first human trials using a drug called SAHA or vorinostat, made by Merck and currently used in cancer treatment, which has shown promise in being able to wake up dormant HIV. As scientists begin to talk up a cure, the old question of whether that’s the right goal has re-emerged. Seth Berkley, a medical epidemiologist and head of the U.S.-based International AIDS Vaccine Initiative (IAVI) is concerned. An HIV-positive person holds a placard during a programme organized to mark World AIDS Day in Kathmandu December 1, 2010. To match Special Report AIDS/ REUTERS/Deepa Shrestha “From a science point of view, it’s a fabulous thing to do. It’s a great target and a lot of science will be learned. But from a public health point of view, the primary thing you need to do is stop the flow of new infections,” says Berkley. “We need a prevention revolution. That is absolutely critical.”   Vuyiseka Dubula agrees. The South African activist finds talk of a cure for HIV distracting, almost disconcerting. “This research might not yield results soon, and even when it does, access to that cure is still going to be a big issue,” she says. “So in the meantime, while we don’t have the answer on whether HIV can be cured or not, we need to save lives.”

Output: Special Report: An end to AIDS?.


Input: Consider Input: Although this therapy is not yet available for patient use, the story makes a point of noting that the cost may well be “stratospheric,” should it make it to market. If approved, such treatments are expected to command stratospheric prices. For example, a separate Spark gene therapy for a rare type of childhood blindness, which is on track for Food and Drug Administration clearance soon, could cost $1 million per patient for infusions in both eyes, according to some Wall Street analysts. Still, the therapies can produce at least some offsetting savings. Porteus noted in his editorial that the hemophilia therapy resulted in savings of about $200,000 a year per patient because of the elimination of clotting-factor infusions. The story summarizes the outcome of the small, 10-person trial that dominates this narrative: Lindsey George, the lead investigator and a hematologist at Children’s Hospital of Philadelphia, said that nine of the 10 men in the trial didn’t experience any bleeding episodes after the gene therapy treatment. The one patient who needed clotting factor because of bleeding used 91 percent less than before, she said. Although the story does not address harms directly–and should have–it does note that one of the worrying side effects of gene therapy—spurring the body to attack itself—was not present in this study. It is clear from the story that the study is small and an “early-stage trial.” One source also notes that the researchers tracked individuals in the study for no more than a year and a half, making longer term assessments unavailable. The story could have done more, though, to signal to the reader that, despite the encouraging outcomes of the study, the treatment is still very much under development. The next stage—Phase 3 trials—requires more participants, more careful study design, and takes, on average, three years to complete. The treatment described here, if ultimately proved worthy, could have a profound impact on a serious genetic condition. Independent sources are identified in the story, as are the funders. But missing from the text is information describing linkages between the two funders—Spark Therapeutics and Pfizer—and the lead researchers. It’s not clear from the story that there is a financial relationship. Individuals coping with hemophilia B have few options, and the story describes the main one: injections of blood-clotting factor to stem runaway bleeding. Since the story notes that the research is at an early stage with only 10 participants, a reader can easily infer that the treatment is not yet available. However, additional information about remaining evaluation stages for this treatment would have been a useful reinforcing addition. Hemophilia B sufferers who see this story will likely be contacting their doctors. The story establishes novelty with this: The researchers presented earlier findings on the gene therapy a year ago at the American Society of Hematology’s annual meeting, but the latest data covers a larger patient group and a longer time period. A news release issued by Children’s Hospital of Philadelphia did a good job of describing this study; the Post story could have picked up more of the salient details from that text but reveals independent reporting nevertheless by including sources not connected to the study.

Output: Gene therapy makes a big advance treating hemophilia B blood disorder


Input: Consider Input: "The story does not address the cost of estrogen plus progestin treatment, nor the costs added or saved due to complications of or benefits from that therapy. However, the story advocates for selective use of low-dose HRT, and only for use in the short-term if menopausal symptoms are bothersome and negatively affect quality of life. The story provides absolute and relative risks of taking HRT for the short and longer term. The story gives number of cases of breast cancer per 1000 women for those who took hormone therapy v. non-users. The story does an excellent job explaining the return to normal lifetime risk of breast cancer if a woman stops taking HRT. The story does not report the results of the JAMA study accurately. There is misplaced emphasis in the story compared with the study. Statements which appear erroneous: ""Even women who took estrogen and progestin pills for as little as a couple of years had a greater chance of getting [all types of] cancer."" There is nothing in this study to contradict the earlier WHI report showing that breast cancer risks start to diverge after about 4 years , not ""a couple of years"". This article reports on all cancers, not just breast. Nowhere in the JAMA article are all cancers plotted over time to support the assertion of a couple of years. Followed by the assertion that ""…these new findings are likely to end any doubt that the risks outweigh the benefits,"" this creates the inaccurate impression that there are new data showing breast cancer risks start earlier on in the course of treatment. A second inaccuracy concerns the statements about the size of the observed risk of breast cancer: ""At the peak, the breast cancer risk for pill takers was twice that of the others."" Not accurate: the hazard ratio was 1.26, indicating a 26% higher breast cancer risk, not 100% higher (which would be twice the risk). Finally, a main point of the article–that cancer risk [presumably all cancer, not just breast] returns to normal roughly 2 years after quitting — is not supported by the study results. JAMA article states ""The HR for overall risk of all malignancies increased from 1.03…to 1.24…in the postintervention period."" And, ""…a downward inflection in the temporal trend in cumulative HRs for breast cancer was observed over time (not shown) but the observed change…is not statistically significant."" The story does an excellent job presenting the latest information from the Women’s Health Initiative on the risk of breast cancer with prolonged use of HRT. The story explains the study design and also interprets the results for the lay reader. Physician interviews put the results of the study in context and reassure women that their risk profile might be different if they are younger or older (women in the study were in their 60’s, typically after menopause is complete), and that their risk should return to normal a few years after stopping a short-term course of HRT. The story does not present menopause as a disease. Based on information on the risks and benefits of HRT for women in their 50’s, the story reiterates the message from the preliminary WHI report, which is that women should make an informed decision with their physician on this treatment option to help manage severe menopausal symptoms. The story reinforces the idea that menopausal symptoms do not require treatment. The story cites several excellent sources, including public health and cancer specialists, who put the results of previous Women’s Health Initiative and this latest information in context. Wyeth Pharmaceuticals is cited on the benefit of HRT in the short-term, and their potential conflict as the maker of Prempro is noted. The story lists HRT as one option for treating very bothersome menopausal symptoms. But other non-medication options are also available, as are non-hormonal drugs used ""off-label"" to ease menopausal symptoms. These are not mentioned. Hormone replacement therapy (HRT) is currently available for women who wish to alleviate particularly bothersome menopausal symptoms, such as hot flashes and vaginal dryness. However, as the story notes, HRT should be used judiciously and only for a short time. The story presents information from the Women’s Health Initiative (WHI) on the increased risk of breast cancer with HRT. The subsequent decline in HRT use after WHI data was made public in 2002 has been linked to a decline in breast cancer cases. HRT is not a new option for treating bothersome symptoms of menopause. It was originally thought that taking estrogen plus progestin treatment could help reduce a woman’s risk of developing age-related heart disease and bone loss. Data from 2002 WHI showed that HRT increased the risk of health disease and breast cancer, and many women discontinued use of this treatment. WHI data discussed in this story reinforce the message that for many women, the risks of HRT outweigh the benefits. There are also other options for managing hot flashes and bothersome menopausal symptoms, which the story does not mention. But for some women, low-dose HRT may still be the most appropriate short-term solution. The story cites several sources and contains independent reporting."


Output: New study firmly ties hormone use to breast cancer