Health Meaning

- Three people dressed in baby suits and blue plastic glasses form a human conveyor belt to chicken embryos . The first has a tray of eggs that were injected with a vaccine against virus yellow fever, and then incubated for 4 days, and cut the top of each egg. The second tweezes embryos on the eggs and places them in a large bottle. The last person added a little liquid and then merges the embryos in a rich red broth that contains millions of weakened virus particles.

The end result of this process, repeated dozens of times each week at the Pasteur Institute in Dakar, is a very effective vaccine that provides lifelong protection against yellow fever . But the 80-year-old process is decidedly low-tech and hard to scale up and that became a problem because a large yellow fever epidemic that began in December 2015 Luanda, capital of Angola, emptied the strategic reserves of the world of vaccine.

Institut Pasteur, which makes about 10 million doses a year, is one of four facilities in the world producing shots for yellow fever, joining two plants operated by the government in Russia and Brazil and french vaccine company Sanofi Pasteur. Their combined production has long been at the height of the world's needs, and the epidemic in Angola has worsened the deficit. Another example of hatching for most in Asia, where yellow fever has never set foot-may be impossible to control, said Jack Woodall, a virologist retired in London, formerly the Centers for Disease Control and Prevention and the World health Organization. "I hate to be an alarmist," said Woodall, who is also a moderator at the Emerging Disease Surveillance System, an online warning system for epidemics. "But this is something I'm really panic about."

vaccine is the only bulwark against yellow fever, a dreaded killer without a remedy that is mainly transmitted through the bite of Aedes aegypti , also known as mosquito yellow fever. Most infected people have no symptoms at all; some experience fever, joint pain and headaches. But progress roughly 15% to a more severe stage in which the eyes and skin turn yellow; they may also bleed from the eyes, nose and mouth. Up to half of these severe cases are fatal. Although yellow fever is endemic in much of Latin America, Africa Door far the heaviest burden. Exact figures are difficult to find, but a study published in 2014 in PLOS Medicine estimated that the disease kills 78,000 Africans each year, although many experts felt that this number was too high.

Most infections occur in or near the jungle where mosquitoes spread the virus primarily between monkeys and sometimes infect a human viewer. urban households, such as Angola, can be much more serious, because mosquitoes can transmit the virus from person to person. "This is when the disease can really take off," said William Perea, the control of the World Health Organization (WHO) department of epidemic in Geneva, Switzerland. Angola has seen 40 confirmed cases and 198 deaths to date, but experts say the real toll could be 10 times higher. "We have not seen an epidemic like this for many years," said Perea.

A massive immunization campaign launched in February has already reached almost 6 million of about 7.5 million people in Luanda. But the disease has since spread to six of the 18 provinces of the country and the overall emergency stock of 6 million vaccines is empty. "This is certainly a stressful situation," said Melissa Malhame of Gavi Alliance for Vaccines, a public-private partnership based in Geneva, which aims to increase immunization in poor countries.

A ramp -up in battle against yellow fever had already stretched global supply of vaccine. many countries have done the shooting part of their routine immunization programs for children, while the catch-up campaigns massive were launched to protect entire populations who never received the vaccine before. a report of the United Nations emergency Fund last year found that the organization needed 42% more vaccines over the next 3 years than is available. A 2013 report put global output in 09 to 75 million doses, against 30 million in 00, but well below the 105 million doses needed this year. Production annual exact day is unknown, but it is probably about 80 million doses, said Tom Monath, a virologist who studied yellow fever for decades and is currently working on NewLink Genetics, a biotechnology company in Ames, Iowa. To make matters worse, the factory in Dakar is about to close for renovation 5 months.

Things can get better in the long run. Demand for the vaccine is expected to decline in a few years after the countries wrap their catch-up campaigns. The Pasteur Institute is building a new facility in Diamniadio, about 30 kilometers from Dakar, which could triple production by 2019; Sanofi Pasteur has built a new factory in France.

Meanwhile the WHO has urged Angola to vaccinate only in areas where yellow fever is spreading. But infected travelers have already made Angola the disease to three other African countries including the Democratic Republic of Congo; if the disease began circulating in its sprawling capital Kinshasa which could be catastrophic, said Monath.

"I think all the specialists in my field agree that there is a real and present danger of having a major yellow fever epidemic that is out of control," adds medical entomologist Paul Reiter of the Pasteur Institute in Paris. " It is a time bomb, "an interim measure could be to reduce the dose of vaccine, Monath said. Some studies have shown that only one-fifth or one-tenth of the current dose may protect people.

spread to Asia is the nightmare scenario for experts from yellow fever. Angola is the many Chinese workers home, and in at least six cases, they have already brought the virus in China. Five of these cases were in Beijing where Aedes aegypti does not occur, so that the disease could not spread. But the mosquito is abundant in southern China and elsewhere in Asia and are therefore vulnerable. Surprisingly, however, yellow fever never took off in Africa.

There a real and present danger of having a major epidemic of yellow fever that is uncontrollable.

Maybe that Asia has just been incredibly lucky. "It has not happened before, but does that mean he's not going to happen now?" Perea request. "Nobody knows."

The worst part of being sick is not always muscle aches and cough. It is the fog head, crankiness, apathy and fatigue in short, what the researchers call the behavior of the disease. A new study reveals a molecular mechanism that explains why we feel so lousy when you're under the weather.

"There is a beautiful study that covered a lot of ground," said neuroimmunologist Colm Cunningham of Trinity College in Dublin who was not connected to the research. "What does that they found is very plausible. "

Although the disease is unpleasant behavior, researchers believe that the symptoms we suffer during a viral or bacterial infection are beneficial, allowing us to turn our energy in the fight against pathogens that have invaded our body. for cancer patients and people with autoimmune diseases, however, the disease's behavior can be an undesirable side effect of treatment with immune molecules called interferons that our cells naturally release when we have an infection.

the condition posed a puzzle for researchers because they assumed the blood-brain barrier, a protective system which excludes most agents pathogens and immune molecules in the brain, could block the immune system signals. Although scientists have identified several mechanisms that allow such messages to cross the barrier behavior and influence, the issue of how the immune system and brain communicate "was only partially answered," said immunophysiologist Keith Kelley of the University of Illinois, Urbana-Champaign, who was not connected to the new study.

to immerse themselves in sickness behavior mechanisms, neuropathologist Marco Prinz of the University of Freiburg in Germany and colleagues exposed mice with a virus that causes a brief illness. The researchers assessed the effects of the pathogen using a standard test for depression in rodents in which the animals are placed in a container of water. Rodents usually struggle to get out of the water, but depressed animals quickly give up and float. Souris has spent almost twice as floating time if they were infected with the virus, suggesting that it affects their behavior.

The researchers found that the virus has stimulated mice to produce a type of interferon, interferon-β. In turn, interferon-β receptor molecules stimulated the protective membranes of the brain and the cells that line the blood vessels of the organ, part of the blood-brain barrier.

To determine whether these receptors trigger the disease behavior, Prinz and his colleagues compared normal mice with genetically modified animals that lack the receptor. After injecting the mice with RNA molecules that trigger the same immune responses as viruses, scientists have rodents with two tests to measure their mental abilities and mood. In the float test, normal mice spent about 50% more time to drift than the genetically engineered mice, the researchers report online today in Immunity , suggesting the animals are more vulnerable to depression if they have the receiver. In a learning test which requires animals to remember the location of a platform in a water tank, RNA injections did not affect the performance of mice lacking receptors. But the normal mouse performance decreased by approximately 50%. "Their cognitive abilities have been massively altered," says co-author Thomas Blank, also a neuroimmunologist at the University of Fribourg.

Prinz, Blank, and colleagues identified two parts of a mechanism that relays immune signals through the blood-brain barrier, but they still need to nail this molecule has caused changes in the brain. they found that in response to interferon-β, the blood vessel cells produce another molecule called CXCL10. the researchers then measured the electrical activity of neurons in the hippocampus, a part of the brain that helps form memories and shapes as our emotions. CXCL10 responses changed in a way that would reduce animal neuron's ability to learn. "We can explain at a cellular level and electrophysiological which is the basis of this [sickness behavior]," said Blank.

the study is important because it identifies a new channel of communication between the immune system and brain, Kelley said. Cunningham added that the data are consistent with the study of his group since last year, which involved the receptor for interferon-β in sickness behavior. But now researchers have gone much further by identifying the role of the interferon receptor in brain areas and revealing the involvement of CXCL10.

neuroimmunologist Robert Dantzer of the University of Texas MD Anderson Cancer Center in Houston is skeptical of the new mechanism, however. "The cytokines produced by immune cells act locally," he said. They are confined to places in the body where immune cells have been fighting against the virus and do not would go to the brain and trigger a disease behavior .

But researchers believe they are on track. An important question now, said Blank, is whether researchers can find ways to stop the behavior of the disease in patients autoimmune disease or cancer that receive treatment with interferon.

What the late pop star Michael Jackson have in common with water buffalo? An incurable skin disorder called vitiligo. In the rare condition, sufferers lose pigmentation and skin becomes blotchy. the cause of Vitiligo is a mystery, although autoimmune disorders may play a role in some cases. Stymieing research was the lack of a good animal model. Now, scientists seem to have found one: the water buffalo. There are four, vitiligo researchers in New Delhi heard a strange tale of social workers. Villagers in a hamlet in western India were shunning the buffalo stomachs rosacea. They hoisted five of last year pariah animals (the one above), and found favor in skin biopsies that bleached buffalo skin spots were a "striking resemblance" to that of human patients with vitiligo. Just as in people, stains buffaloes had vanishingly few melanocytes pigment bearing cells and low levels of gene expression of pigmentation, reports the online team in the journal Pigment Cell & Melanoma Research . The New Delhi team wasted no time making use of the new animal model. In buffalo, stains have spread "confetti-like" tail of the animal to its rump and face in just 6 months; researchers are testing a new compound to see if they can stop the spread.

Researchers who want to treat illnesses carrying a gene into cells are often faced with the obstacle the introduction of DNA into them securely enough to make a difference. Now scientists have developed a new way to genetically modified cells in the liver take over much of this body: They paralyze the unmodified cells. This strategy seems risky, based on the exceptional regenerative powers of the liver, has passed its first test in mice. If so successful in people, it could be a boon for the treatment of many inherited diseases involving the liver.

"This is very good proof of concept. The authors [of the new study] would be the first to admit he still has a way to go, but it is a very exciting step in my opinion," said Ian Alexander of the University of Sydney in Australia, working on gene therapy for liver disease in children.

Gene therapy shows promise for several rare diseases including hemophilia B, in which people do not have a protein called factor IX livermade that helps blood clot. Some researchers and companies currently use a so-called vector, the harmless adeno-associated virus (AAV), to transport in liver cells a DNA loop with a working copy of the factor IX gene.

But the treatment has its limits. So far it has not given patients with hemophilia B enough factor IX to completely prevent bleeding episodes, they need about 12% of normal levels, but get half or less with therapy. And those treated with higher doses sometimes need a steroid medication to counter an immune response to the virus. For many other liver diseases, a similar AAV gene therapy would not change enough cells, or maintain a sufficiently high activity of the new genes to produce the necessary amount of protein. And in children, these therapies may lose their effectiveness as the liver and the modified cells develops lose the loops of the foreign DNA.

But the human liver's ability to regenerate offers another strategy. Remove three-quarters, and it will be renewed quickly. Knowing this ability to rebound, Sean Nygaard and others in the laboratory of gene therapy researcher Markus Grompe liver Oregon Health & Science University in Portland and colleagues at Stanford University in Palo Alto, California, sought to stimulate the production of the foreign gene by giving liver cells modified two important changes. First, instead of using AAV to produce DNA loops in the cell, they conceived an AAV to integrate into the human factor IX gene into a chromosome of the cell, close to another gene which leads expression, so that the foreign DNA is not lost as cells divided. AAV also carried DNA encoding a short strand of RNA that blocks an enzyme that makes liver cells undergo DNA damage and stop dividing when exposed to a drug called CEHPOBA.

in mice healthy newborns who received an injection of AAV in the liver, followed by daily injections of CEHPOBA for 4 weeks, modified liver cells multiplied to replace those with disabilities. As it happened, the mice blood levels of human factor IX has increased well above the level of a patient with hemophilia B would need 10 to 30-fold higher than in mice that received therapy gene, but not CEHPOBA, reports the team today science Translational Medicine . Depending on liver disease, adjusting doses of CEHPOBA, Grompe said, "you can dial in how much the factor IX [or other protein] you wanted."

But the dangers of using a drug to deliberately injure the liver cells? Grompe said that is not as risky as it sounds because babies are sometimes born with a condition that mimics harmful liver effects of the drug CEHPOBA. Still, they can completely recover if treated. "We have the natural history of what happens to these patients as an argument to say you can do it," said Grompe. And although CEHPOBA is not an approved drug, his team thinks he can get the same results using RNA that confers resistance to a common drug that is toxic to the liver, as the analgesic acetaminophen.

Kathy High, President of Spark Therapeutics, a gene therapy company in Philadelphia, Pennsylvania, called the new "smart" strategy, but it is wary of hurting liver cells deliberately. His company is working on an improved AAV treatment at low doses gave three patients with hemophilia B to 30% of the activity factor IX of healthy people. "There are other ways to do it," she suggests. Yet she and Alexander say it is wise to approach the problem from many angles, because it is difficult to predict what will work best in people. "My experience over many years is that of trying to work on several different strategies is generally a good thing," said High.

Researchers who want to treat illnesses carrying a gene into cells are often faced with the obstacle the introduction of DNA into them securely enough to make a difference. Now scientists have developed a new way to genetically modified cells in the liver take over much of this body: They paralyze the unmodified cells. This strategy seems risky, based on the exceptional regenerative powers of the liver, has passed its first test in mice. If so successful in people, it could be a boon for the treatment of many inherited diseases involving the liver.

"This is very good proof of concept. The authors [of the new study] would be the first to admit he still has a way to go, but it is a very exciting step in my opinion," said Ian Alexander of the University of Sydney in Australia, working on gene therapy for liver disease in children.

Gene therapy shows promise for several rare diseases including hemophilia B, in which people do not have a protein called factor IX livermade that helps blood clot. Some researchers and companies currently use a so-called vector, the harmless adeno-associated virus (AAV), to transport in liver cells a DNA loop with a working copy of the factor IX gene.

But the treatment has its limits. So far it has not given patients with hemophilia B enough factor IX to completely prevent bleeding episodes, they need about 12% of normal levels, but get half or less with therapy. And those treated with higher doses sometimes need a steroid medication to counter an immune response to the virus. For many other liver diseases, a similar AAV gene therapy would not change enough cells, or maintain a sufficiently high activity of the new genes to produce the necessary amount of protein. And in children, these therapies may lose their effectiveness as the liver and the modified cells develops lose the loops of the foreign DNA.

But the human liver's ability to regenerate offers another strategy. Remove three-quarters, and it will be renewed quickly. Knowing this ability to rebound, Sean Nygaard and others in the laboratory of gene therapy researcher Markus Grompe liver Oregon Health & Science University in Portland and colleagues at Stanford University in Palo Alto, California, sought to stimulate the production of the foreign gene by giving liver cells modified two important changes. First, instead of using AAV to produce DNA loops in the cell, they conceived an AAV to integrate into the human factor IX gene into a chromosome of the cell, close to another gene which leads expression, so that the foreign DNA is not lost as cells divided. AAV also carried DNA encoding a short strand of RNA that blocks an enzyme that makes liver cells undergo DNA damage and stop dividing when exposed to a drug called CEHPOBA.

in mice healthy newborns who received an injection of AAV in the liver, followed by daily injections of CEHPOBA for 4 weeks, modified liver cells multiplied to replace those with disabilities. As it happened, the mice blood levels of human factor IX has increased well above the level of a patient with hemophilia B would need 10 to 30-fold higher than in mice that received therapy gene, but not CEHPOBA, reports the team today science Translational Medicine . Depending on liver disease, adjusting doses of CEHPOBA, Grompe said, "you can dial in how much the factor IX [or other protein] you wanted."

But the dangers of using a drug to deliberately injure the liver cells? Grompe said that is not as risky as it sounds because babies are sometimes born with a condition that mimics harmful liver effects of the drug CEHPOBA. Still, they can completely recover if treated. "We have the natural history of what happens to these patients as an argument to say you can do it," said Grompe. And although CEHPOBA is not an approved drug, his team thinks he can get the same results using RNA that confers resistance to a common drug that is toxic to the liver, as the analgesic acetaminophen.

Kathy High, President of Spark Therapeutics, a gene therapy company in Philadelphia, Pennsylvania, called the new "smart" strategy, but it is wary of hurting liver cells deliberately. His company is working on an improved AAV treatment at low doses gave three patients with hemophilia B to 30% of the activity factor IX of healthy people. "There are other ways to do it," she suggests. Yet she and Alexander say it is wise to approach the problem from many angles, because it is difficult to predict what will work best in people. "My experience over many years is that of trying to work on several different strategies is generally a good thing," said High.

A Wednesday morning in April, a line of 0 people infected with HIV winds through the corridors of the first room waiting clinical Themba Lethu, a wing of the hospital Helen Joseph in Johannesburg, South Africa. In most places in the country, where clinics are overtaxed, it presages a wait of up to 10 hours. But here's something different happens. Staffers at computer screens quickly connect in people and ship them for sorting or, if they have tuberculosis, a special area away from others. Those who are not their (ARVs) for antiretroviral drugs to walk directly to pharmacists, recovering electronic medical record of each patient and use a robotic system to take medication tablets and fill orders. The average waiting time is 30 minutes to 2 hours for a visit to the doctor or nurse and 15 minutes to the pharmacy. An ATM prototype promises to continue the rate of visits by distributing directly ARV pills; one day, hopefully, similar pills machines in malls could make a few visits to the clinic useless.

"This is an awesomely efficient place," said Ian Sanne, head right to care, a nongovernmental organization that works this and several other clinics in collaboration with the Ministry of Health. In developed countries where patients complain about waiting much shorter, this bravado may seem absurd. But in South Africa, Themba Lethu Clinic is celebrated as an example of what can be done to take care of a large number of people infected HIV. This is both a compliment to the clinic and a hint of overwhelming challenge of HIV / AIDS in the country.

South Africa has promised to step up efforts to end its huge HIV / AIDS, the largest in the world. Come September, it will offer all ARVs infected person, which both ward off illness and make people less infectious. the immediate objective is to achieve what is known 0-0-0 as 2020: to have 0% of infected people know their status, 0% of known positives start ARVs, and 0% of this group lead the amount of virus in their bloodstream to undetectable levels. The theory is that the viral load drops, the transmission, too, leading the epidemic spiral downward. The 0-0-0 target is the cornerstone of a great campaign, articulated by the United Nations Programme on HIV / AIDS (UNAIDS) and widely adopted by world leaders to end the AIDS epidemic "as a threat to global public health" by 2030.

in a nation estimated at least 6.6 million people in 18 HIV-infected% of the world total-player to hit 0- 0-0 2020 seems too ambitious to many experts. and the obstacles faced by South Africa provide a reality check sobering to high laudable aspiration to end AIDS, a topic that promises to occupy a central place later this month in Durban at the biannual international AIDS Conference.

models and reality

a model predicts how the various response scenarios to HIV / AIDS would affect infection rates, or impact. As seen on the map, some regions have many more HIV than others.

South Africa has made huge gains against the HIV epidemic / AIDS. During his last hosted this international meeting in 00, then President Thabo Mbeki and his health minister have questioned whether HIV causes AIDS even, sparking widespread outrage. At the time, only the wealthiest South Africans had access to ARVs, which cost about $ 5,000 per person for an annual supply. But at the end of 2015, the price had dropped to $ 100, and 3.4 million HIV-positive South Africans were receiving ARV-more than in any other country in the world. South Africa, in fact, consumes the same amount of drugs vital importance that Asia and the Pacific, North America, and Western and Central Europe combined.

Consequently, life expectancy jumped 9 years between 05, when ART started to become widely available, and 2014. The country has developed innovative ways to deliver medications and assist people stay on them. And strong team of South African researchers on HIV / AIDS has made the country a hub of cutting-edge basic research and clinical trials. "Given our resources, we have done amazing things," says Glenda Gray, a researcher on HIV / AIDS who heads the Medical Research Council of South Africa in Cape Town

yet nearly half of the infected population today is still treated. Some have not suffered enough damage to the shelter of the virus to deserve ARVs in the current policy framework of the government. Many others infected do not know their status or never seek treatment, and others entering treatment have difficulty taking their daily pills for years. According to estimates, due to flaws in this "continuum of care", only one in four South African HIV has completely removed the virus. "We must ride two horses at the same time," says Fareed Abdullah, who heads the quasi-governmental South African Council National AIDS (SANAC) in Pretoria. "One is to improve our system so that more than 3 million on treatment are kept in the care and well managed, and we also extend to a group that is in large part asymptomatic and well."

Adding to those challenges is alarming HIV incidence-the percentage of the South African population becoming infected each year. the Government indicates that HIV incidence has fallen from a high of 1.67% among adults in 05 to 1.22% last year, but that still translates into 330,000 new infections per year. the rate is extremely high among women under 25, particularly in the most affected province, KwaZulu -Natal, where the incidence tops 6% in some communities.

Health Minister Aaron Motsoaledi, who acknowledges that aggressive HIV / AIDS country program had a late start because of Mbeki, is convinced that South Africa has the will and the money to knock 0-0-0. "Can we afford not to treat people?" Application Motsoaledi. "Certainly, we will pay much more socially, politically and economically if you can not." To this end, the government, which already spends $ 1.2 billion annually on HIV / AIDS and gets another $ 300 million in foreign currency support, is adding $ 65 million per year until 2019 .

But a new report concludes that to achieve the objective of UNAIDS will require an additional $ 8 billion over the next five years. "UNAIDS pushing very hard on our health ministry, which does not yet caughtshort and wants to make the case that we can achieve 0-0-0" said Linda-Gail Bekker, who co-directs the Desmond Tutu HIV Foundation (DTHF) in Cape Town and is one of the co-authors of the report. The cost of drugs is just part of the equation, she said. To achieve the goal will also require massive HIV testing and costly provision of ARVs to patients should be monitored and helped if they do not remove the virus. "I'm really, really worried about the resources it will take."
There are scientific questions, too. The assumption that to reach the goal 0-0-0 ending AIDS is based on mathematical models that take into account the "cover" ARV in combination with other proven prevention strategies such as male circumcision, condom promotion and behavior change efforts. the researchers note that in large epidemics such that in South Africa, which exceeded the population "concentrated" as men who have sex with men and sex workers, such strategies might prove less effective than expected, allowing HIV to continue disseminating high levels even after the country achieved 0-0-0.

Epidemiologist Salim Abdool Karim, director of the Centre for AIDS Programme of research in South Africa (CAPRISA) in Durban, points of recent data from Botswana who question the assumptions of the model. Botswana, which is relatively rich and has a small population of 2 million, has almost reached 0-0-0, as shown in a study published online March 23 in The Lancet. But the impact has barely moved, in part because the missing 10-10-10 continue to spread the virus. "For a country that is close to 0-0-0, the incidence is ridiculously high," Karim said. "It is outrageous." A report published by the Ministry of Sanac and other health issues of mathematical modeling 0-0-0. Although 0-0-0 led to sharp declines in new infections in 2030, this report suggests that the incidence in the population of South Africa's 53 million will not quite go below 0.1 % -the level as UNAIDS says it needs to reach to an epidemic in the end.

The bottom line is that it remains an open question whether the treatment 0-0-0 goal can really stop the spread of HIV in South Africa. Some of the biggest global controlled treatment trials as prevention (TasP) are underway in the country to try to answer.

in a region known as the Mfekayi in rural KwaZulu-Natal, two dozens of people sat on the shaded porch of a cabin plywood waiting their turn to see a counselor. The cabin is Egedeni Clinic, and people are participants in a 28,000 person, multi-site clinical trial that will assess the precise relationship between increasing levels of HIV suppression in a community and the impact of declines. A Egedeni and 10 other clinics throughout the province, TasP study provides ARVs to all infected participants. 11 other clinical tASP offer instead of the treatment according to current recommendations of the government, which means that people start ARV only after their immune system show signs of damage.

One by one, participants bottles by hand ARVs they received a month earlier to counselors, who count the remaining pills. This ritual, which is a crude way to monitor compliance underlines an obvious limitation of the underlying strategy: Although ARVs make people less infectious, TasP based on human fickle relationship have with medication daily.

Managed by the African Centre for Population Health around Mtubatuba, TasP is the longest of the four similar trials in sub-Saharan Africa that examine the continuum of care and outcomes of real world 'universal treatment. "Preliminary analysis of the results tASP found that less than 40% of those who tested positive have sought care within 3 months, as recommended. This first step has always been a major obstacle on the road to 0- 0-0.

at the international AIDS Conference later this month, the researchers plan to reveal whether their intervention helped to reduce the impact. "this will be the first opportunity assess whether, in fact, the purpose of bio-logic is actually true in practice, "says Deenan Pillay, a clinical virologist who heads the Africa Centre. But Pillay said the study has already clarified that the end of AIDS is not simply a matter of "we will treat everyone and everything will be OK." In the final analysis, he said, the power depends as much TasP on human behavior as it is about biology.

Jacqualine Ncube, a restaurant worker of 19 years, first took an HIV test when she was in high school. at the time, Ncube spent many hours after school to hang out at DTHF youth Center, adjacent to the town of Masiphumelele fight outside Cape town. the youth Centre offers internet access of adolescents, holds football matches, boards of loans surfing, and provides care in a health clinic. children also earn "Tutus" good for vouchers or food for every-thing to help the community to take an HIV test. When Ncube obtained its first results, she was overwhelmed. "I really cried," she said. It was negative.

Ncube has tested negative several times, and in April 2015, she joined Pillsplus Youth Centre, a study of what is known as pre-exposure prophylaxis, or PrEP, in 150 adolescents. With PrEP, uninfected people take pills daily ARVs to prevent infection. Although PrEP is a proven strategy, South Africa recommends its use in sex workers, and Ncube is one of the first hetero-sexual adolescents worldwide on ARVs for prevention. She always uses condoms with her boyfriend, but said she wanted to try PrEP because "no 100% protection."

of DTHF Bekker, head Pillsplus to assess the acceptability of PrEP among adolescents, argues that PrEP must be provided to all people at high risk of infection. "When I sit in front of a 17-year-old young woman, I have nothing to offer," says Bekker.

Karim said CAPRISA PrEP among young women could be the key to break the back of the epidemic. About 30% of new infections in South Africa occur in young women between 15 and 24 years. the new infection rate among men in the same age is over four times lower. in some districts of KwaZulu-Natal, a woman has a chance of being infected by age 34. 60%

Gender and age

HIV infects more girls and young women and boys and men of the same age in South Africa. the gender difference narrows to 35 years, while the prevalence drops.

to understand the viral spread scheme, and the African Centre CAPRISA mapped on the cycle of infection between men and women of different ages in KwaZulu-Natal . The study analyzed the genetic sequences of HIV isolated from 858 men and women, all aged between 16 and 35, who belonged to the same sexual networks. different isolates associated viral genetics and said those who were older, which allows researchers to deduce who infected whom. Teenage girls were infected by men who were on average 8 years older. After age 24, people in general were infected by partners of their age, with the transmission shift more often from women to men. "They try to find life partners at this age," says Karim. These older men are the same group who have sex with younger women. "We need to break the chain of men in their late 20 and teen girls, "he said.

PrEP can help TasP address gaps, said Karim. in the study infection cycle, men who infected young women had extremely high levels of HIV, indicating that they have recently acquired the virus and does not seem infected on standard antibody-based tests. "If your strategy is to test and treat people, you do not going to catch them, "says Karim. men are also less connected to the health care system and often migrate for work, he adds, making it more difficult to help those who know they are infected completely remove the virus. Giving young women PrEP prevents the male dilemma. "We just have to protect girls for 5 years in this period of critical risk until they find their partners," he said.

Karim said new biomedical interventions the horizon may strengthen prevention efforts. His group plans to report to the Durban meeting that identified a microbe related to unusual vaginal inflammation in women in KwaZulu-Natal. Treat it could potentially reduce their risk of HIV infection. injectable ARVs that last two months are also tested in South Africa and elsewhere, and those that could eliminate the challenge of taking pills, daily key problem for the treatment and PrEP. Next fall, South Africa plans to launch trial of effectiveness in the world with a stronger vaccine AIDS preventive medicine of all.

For now, 0-0-0 is the most powerful tool available in South Africa in its quest to end the epidemic, even if PrEP and other emerging strategies are needed ultimately. Abdullah SANAC has a pragmatic vision to meet the deadline of UNAIDS. "I think we should plan, because if we do not get it by 2020, we'll do it in 2022," he predicted. "What we're really after is lowering new infections to levels low, "and to get the largest number of people infected with HIV as possible on treatment and live a longer life. the virus itself Abdullah said," will be with us for the next 100 years. "

the Pulitzer Center on crisis reporting provided support for the reporting in this story.

for science the coverage on HIV / AIDS, visit our topic page.

in this week's podcast, Jon Cohen speaks with Julia Rosen about South Africa to end AIDS.

Humans Did not evolve alone. Tens of trillions of microbes-have Followed us on our journey from prehistoric ape, Evolving with us along the way, selon a new study. Aim the work finds aussi That We've lost Reviews some of the ancient microbes That still inhabit our great ape cousins, qui Could explain Some human diseases and obesity-even and mental disorders.

Researchers Have Known for Some Time That humans and Reviews the other great apes harbor Many kinds of bacteria, Especially in Their guts, a collection Known as the microbiome. Aim where did come from microbes thesis: our ancient ancestors, or our environment? A study of fecal bacteria across all mammals suggéré que la microbes are More Likely to be inherited than Acquired from the environment. Purpose --other studies-have found That diet plays a major role in shaping the bacteria in our guts.

To solve the mystery, Andrew Moeller turned to wild apes. As share de son doctoral dissertation, the evolutionary biologist, now a postdoc at the University of California, Berkeley, Studied gut bacteria isolated from fecal samples from 47 chimpanzees from Tanzania, 24 bonobos from the Democratic Republic of the Congo, 24 gorillas from Cameroon, and 16 humans from Connecticut. In dissertation samples, he and colleagues at the University of Texas (UT), Austin, Compared the DNA sequences of a single gene Rapidly Evolving That Is common in the gut bacteria in apes, Including humans. Then They sorted the different DNA gene sequences into family trees.

It turns out That MOST of our gut microbes-have-been Evolving with us for a long time. That Moeller found two of three major families of gut bacteria in humans and apes traces Their origins to a common ancestor more than 15 million years ago, not to bugs Primarily picked up from Their environment. Goal as the different species of apes diverged from this ancestor, Their gut bacteria aussi split into new strains, and coevolved in parallel (a process Known As cospeciation) to adapted to differences in the diets, habitats, and diseases in the gastrointestinal tracts of Their hosts, the team reports today in Science . Today, thesis microbes are finely adapté to help process our immune systems, guide the development of our internal, and-even modulate our moods and Behaviors.

"It's surprising That our gut microbes, qui We Could get from Many Sources in the environment,-have Actually beens coevolving inside us for Such a long time, "says project leader Howard Ochman, an evolutionary biologist at UT Austin.

After the ape species diverged, some aussi lost distinct strains of bacteria That PERSISTED in --other primates Likely Reviews another sign of adaptation in the host, the team found.

in a final experiment, the Researchers probed deeper into the human microbiome. They Compared la même DNA sequence They HAD Analyzed in all of the apes, the goal this time between people from Connecticut and people from Malawi. They found bacterial strains from que la thesis Africans diverged from Those of the Americans about 1.7 million years ago, qui corresponds with the Earliest exodus of human ancestors out of Africa. This Suggests That gut bacteria can be used to track animal and early human migrations, Moeller says. Interestingly, the Americans lacked Reviews some of the strains of bacteria found in Malawians-and in gorillas and chimps-which fits with the general reduction in gut microbiome diversity That has-been Observed in people in Industrialized societies, Perhaps Because of exchange in diet and the use of antibiotics.

The work "Represents a significant step in understanding human microbiota coevolutionary history," says Justin Sonnenburg of Stanford University in Palo Alto, California, Who was not Involved with the research. "It elegantly shows That gut microbes are Passed Vertically, entre generations over millions of years." Microbiologist Martin Blaser of New York University in New York City Chartered: "The path of transmission Was from mom apes to baby apes for Hundreds of Thousands of generations at least. "

aim the extinction of Some strains of bacteria persist in --other That apes but not humans raises a red flag for our health. "What happens if a human mom takes antibiotic When She's pregnant? What happens if she takes it at the time of delivery? "Asks Blaser.

" We are coming to Understand how Fundamental our gut microbes are for health, "Sonnenburg says. "These Findings-have huge implications for how we shoulds Pursue understanding what a truly healthy microbiome looks like."

* Correction, July 21, 2:34 pm: The headline of this article has-been updated to correctly indicate indication an editing error and the microbes-have-been with humans for millions of years.

Scientists say they have for the first time examined the blood of a mother for genetic signs of disease in the fetus. The technique could one day offer an alternative to invasive methods of prenatal diagnosis such as amniocentesis and chorionic villus sampling (CVS), which slightly increases the risk of miscarriage.

Yuet Wai Kan and colleagues at the University of California, San Francisco, extract fetal cells from maternal blood to see if the fetus had the genes for two recessive diseases: sickle cell anemia and a similar condition called beta thalassemia. Their findings are published in the November Nature Genetics .

The method relies on the fact that a handful of fetal blood cells leak into the blood of the mother through the placenta. Scientists have isolated the fetal red blood cells in the blood of two pregnant women, each carrying one of these diseases. They stained cells with an antibody directed against a fetal protein and plucked with a small needle. Standard DNA analysis revealed that neither had inherited both copies of the gene necessary to develop symptoms, and CVS tests confirmed the results. One drawback, Kan said, is that the test does not work on fraternal twins as he can not discern what fetal cells come.

A noninvasive test performed in early pregnancy would be "very attractive" for many women, says Mary Mahowald, a bioethicist at the University of Chicago. But first, this procedure should be more people vetted. "We have shown that this is possible," said Kan, "but we need other tests to show how accurate it is."

A new vaccine can prevent dangerous infections among infants and their mothers. A vaccine against group B streptococcus (GBS) - which causes severe infections in nearly two 1,000 newborns and kills about 10% of infected people - triggered the production of antibodies against the bacteria in tests clinical

vaccines work. by exposing the body to a lure representing an infectious agent, so that when the real pathogen comes along the body will see a resemblance and mount an attack. The recognizable part of GBS is a complex sugar coating, which immunizes only about 60% of people. To make a vaccine that can protect most of the rest, infectious disease expert Dennis Kasper and colleagues at Brigham and Women's Hospital in Boston used a relatively new technique to connect the complex sugar tetanus toxoid, a protein known to elicit a strong immune response.

conjugate vaccine seems to do the trick, triggering levels of protective antibodies in 54 of the 60 women tested, with no serious side effects. The killed GBS antibodies in the test tube, and, at least in mice, were able to cross the placenta and fetus immunize. After Kasper researchers injected pregnant mice with antibodies from immunized women, mouse gave birth to puppies immune to GBS. "The characteristics of the antibody were what we expected, '' said Kasper, who with Carol Baker of Baylor College of Medicine in Houston in detail the clinical trial in the latest issue of Journal of Clinical Investigation .

conjugate vaccine is the first demonstrated both safe and effective, said Pamela McInnes, project manager for the Initiative streptococci group B at the National Institute of allergy and infectious diseases . More human trials are needed, especially to see if the vaccine is safe for pregnant women McInnes said the vaccine also offers the promise to reduce the number of reproductive age women carrying GBS - now estimated at 10 .. % to 30% of the search can now, she said, "with a more clinical approach and with real hope for prevention. ''

A new vaccine can prevent dangerous infections among infants and their mothers. A vaccine against group B streptococcus (GBS) - which causes severe infections in nearly two 1,000 newborns and kills about 10% of infected people - triggered the production of antibodies against the bacteria in tests clinical

vaccines work. by exposing the body to a lure representing an infectious agent, so that when the real pathogen comes along the body will see a resemblance and mount an attack. The recognizable part of GBS is a complex sugar coating, which immunizes only about 60% of people. To make a vaccine that can protect most of the rest, infectious disease expert Dennis Kasper and colleagues at Brigham and Women's Hospital in Boston used a relatively new technique to connect the complex sugar tetanus toxoid, a protein known to elicit a strong immune response.

conjugate vaccine seems to do the trick, triggering levels of protective antibodies in 54 of the 60 women tested, with no serious side effects. The killed GBS antibodies in the test tube, and, at least in mice, were able to cross the placenta and fetus immunize. After Kasper researchers injected pregnant mice with antibodies from immunized women, mouse gave birth to puppies immune to GBS. "The characteristics of the antibody were what we expected, '' said Kasper, who with Carol Baker of Baylor College of Medicine in Houston in detail the clinical trial in the latest issue of Journal of Clinical Investigation .

conjugate vaccine is the first demonstrated both safe and effective, said Pamela McInnes, project manager for the Initiative streptococci group B at the National Institute of allergy and infectious diseases . More human trials are needed, especially to see if the vaccine is safe for pregnant women McInnes said the vaccine also offers the promise to reduce the number of reproductive age women carrying GBS - now estimated at 10 .. % to 30% of the search can now, she said, "with a more clinical approach and with real hope for prevention. ''

In a surprising finding, daily supplements of the trace element selenium have been found to reduce the risk of several types of cancer in patients with skin cancer history. The results, reported in tomorrow's issue of Journal of the American Medical Association , surprised researchers, which discourage people from loading the supplement until the results are replicated in other people .

A team led by epidemiologist Larry Clark of the Arizona Cancer Center in Tucson had observed lower rates of skin cancer in people with high levels of selenium. So the group has undertaken to test whether selenium could reduce the risk of recurrence of basal cell or squamous cell carcinoma in people previously treated for skin cancer. Beginning in 1983, they began to enroll patients from seven dermatology clinics in the eastern United States, giving half the group a placebo daily and the other half to 0 micrograms of selenium beer yeast tablet. A total of 1312 patients, three quarters were men, received selenium or placebo for an average of 4.5 years.

The group found that selenium was no better than placebo in preventing a return of skin cancer, refuting initial thesis. But he demonstrated some anticancer properties. For example, the selenium group recorded only 77 cases of secondary cancer compared with 119 in the control group. For prostate cancer, the ratio was 13 cases vs. 35; for colorectal cancer, eight against 19; and for lung cancer, 17 against 31. The selenium group also experienced 17% fewer deaths, including half the number of tests from a variety of cancers. The trial was to continue for 2 years, but Clark pulled early decision "so that doctors can know of this potential for cancer prevention."

Experts say the results should be considered with caution. the study is "very, very encouraging," said Clement Ip, a cancer researcher at Roswell Park cancer Institute in Buffalo, but he and others say more studies are needed to determine how selenium affects tumors . and how it affects a broader spectrum of patients There are also questions about its safety when taken on a long term basis: Selenium can lead to hair loss and nail doses above 1 milligram . "We recommend that we do an additional test to confirm these results and see how it spread to other people," said Clark, especially women and people with certain types of cancer.

Scientists have created a new species of mouse suffering from atherosclerosis when fed a Western diet rich in fats. The discovery, reported in Science tomorrow * offers a model for probing the causes of a human disorder - familial combined hyperlipidemia (FCHL) - which occurs in about 2% of people in Western countries and can lead to premature coronary heart disease.

In a simple and elegant experience, Alan R. Great and his colleagues high mouse Columbia University with a human gene linked to FCHL with mice lacking receptors for several proteins that bind to low density lipoprotein ( LDL), a fat molecule to which elevated blood levels is associated with atherosclerosis. The human gene, apolipoprotein C-III is linked to high blood levels of low density lipoprotein (VLDL), also a culprit in heart disease. Thus, the offspring of mice had the worst of both worlds :. VLDL and expenses of a crippled ability to remove LDL circulating blood

Tall team fed mice a diet consisting of approximately 20% saturated fat which was also high in cholesterol. "The big surprise," said Grand, "is that both genetic defects do not simply add to each other. They were clearly synergistic." The mice four times the normal normal levels of VLDL and LDL compared to mice developed arterial clogging and earlier and more severely than did mice and genetically modified food on a regular hybrid. The finding adds weight to a theory that APOC3 and defective LDL receptors play a key role in all the high lipid levels observed in FCHL says Grand.

"There is an imaginative study," says Richard Havel, a lipid researcher at the University of California, San Francisco. But APOC3 is probably not the only villain in FCHL, which is considered from defects in several genes. yet, Havel said, the work "is a step in the right direction." the next step will be to try to breed mice with defects in several genes that mimic the human condition more closely.

* Science online subscribers can link to the full text of the report.

A protein that triggers the growth of blood vessels appears to play a key role in the development of Kaposi's sarcoma. The discovery, published in the tomorrow of the Proceedings of the National Academy of Sciences, may lead to better treatments for the disfiguring and potentially fatal cancer that strikes nearly a third of AIDS patients.

pathologist Parkash Gill and his colleagues at the University of Southern California School of Medicine had suspected that vascular endothelial growth factor (VEGF), a protein that regulates the permeability of blood vessels and stimulate growth, could be involved in Kaposi's sarcoma, because tumors - that appear as purple spots on the skin - twisted masses of disorganized blood vessels and capillaries that leak. The team found that the Kaposi sarcoma cells indeed produce scads of VEGF. They also noted that tumor cells with elevated levels of two receptor proteins that bind to VEGF, whereas the skin cells from the adjacent unaffected areas had no receptors.

Gill group next tried to block VEGF with the hope of preventing tumor growth. They injected with antisense DNA - a mirror image so of the DNA segment in the gene encoding the VEGF protein - into mice with tumors. The antisense DNA can bind to the cell an RNA template for the protein, thus strangling its production. The treatment seems to work :. Tumors in mice that received the antisense DNA has not increased as rapidly as those mice that received random DNA fragments

"If it holds up that VEGF is an very central player "in Kaposi sarcoma, said Harvard University cell biologist Judah Folkman, it may open multiple avenues of treatment. Although the initial antisense DNA tests were promising, Gill said compounds that block VEGF receptors can also be a weapon against cancer, which can kill patients when tumors invade the lungs or other organs.

BETHESDA, MARYLAND NCI-tU-Turn on mammograms - Cancer The National Cancer Institute (NCI) has once again breast approved test for women in their forties. The action brings NCI's recommendations in line with those of the American Cancer Society and other groups, but puts the body against external scientific group recently concluded that these tests save Lives.

At a press conference today, the National Advisory Council of Cancer (NCAB) announced its support for mammograms every 1 to 2 years for women aged 40 to 49 with a normal risk breast cancer. These X-ray tests could save lives per year 1500-00, says NCI Director Richard Klausner, although the board noted that a third of all diagnoses may be false alarms. Klausner welcomed the recommendation of the Board and said the policy would become effective immediately.

Although most experts agree that regular mammograms can reduce breast cancer deaths among women over 50, they have fiercely debated the value of universal screening for women in their forties . Clinicians who treat breast cancer patients are among the staunchest supporters of screening, while many epidemiologists find little statistical evidence for a benefit. In 1993, citing a lack of clear scientific evidence, NCI reversed its policy and decided not to recommend screening in this age group. In January, a panel of 14 members of epidemiologists side and reiterated this position after having evaluated seven randomized trials.

But the NCAB came to a different conclusion, deciding that mammograms every 1 to 2 years to reduce breast cancer mortality by about 17%. The advantage is "difficult to detect with a high degree of certainty," admitted President NCAB Barbara Rimer, a behavioral scientist at Duke University, but adds that universal screening is "scientifically defensible." The only dissenting voice on the board of 17 members was epidemiologist Kay Dickersin of the University of Maryland School of Medicine.

The new policy does not apply to women in their forties with a high risk of breast cancer, those family history of the disease, certain genetic mutations, or who gave birth after age 30. These women said the council should consult a physician for the appropriate interval for testing. The board made its decision a month earlier than planned because of public controversy stirred by the position of the consensus group, Rimer said, but it did not influence the result. "We made our separate work all this "ACS officials applauded the new NCI policy and said it was in line with its recommendation for annual screening in this age group.

low-tar cigarettes can reduce your chances of getting a type of lung cancer, but they increase your risk of another type of lung cancer, according to a study reported in next month's issue of cancer . The work, carried out in Switzerland, supports the prevailing belief that low tar cigarettes are not much safer than their predecessors high octane.

Fabio Levi of Vaud tumor registry in Lausanne, Switzerland, and colleagues analyzed 7423 cases of lung cancer reported between 1974 and 1994 in two Swiss states, Vaud and Neuchâtel. The group found that the incidence of squamous cell tumors in larger lung tubes in men fell 27% from 1974 to 1979 in 1989-1994. Meanwhile, the rate of adenocarcinoma, which affects cells secreting mucus from the lungs, increased by 142% over the period. Overall, the rate of lung cancer in the region increased slightly, from 55.6 to 57.5 cases per 100,000 people.

Swiss researchers blame the cancer rates of lung shift on phase-in since the mid-1950s to mid '80s cigarettes containing lower tar, which is rich in carcinogens. Therefore, they say, smokers have less tar deposits in major pulmonary tubes, which represents the rate of less tumor there. But the smoke low tar cigarettes is easier to breathe and tends to get sucked deep into the lungs. Levi's group suggests that this deep breathing offers more carcinogens in smaller pulmonary branches, where adenocarcinoma develops

The authors acknowledge that other factors -. dietary changes to air pollution - can be at least partly responsible for the shift in the type of lung cancer. Nevertheless, the study confirms similar trends in US cancer rates, said Neal Benowitz, a researcher of nicotine at the University of California, San Francisco. Switching to low-tar cigarettes, he said, can reduce the risk of certain diseases, but it will not protect you against the real killers: "You will not change your risk of cancer or heart disease. "

SAN FRANCISCO - A therapeutic vaccine against severe rotavirus diarrhea, which kills nearly 00,000 children worldwide each year, succeeded in clinical trials. The vaccine works best "to mitigate the outcome of the disease" - not necessarily to prevent it, said Hsieh Chia-Lung, Senior Director of Vaccine Development at Wyeth-Lederle Vaccines and Pediatrics. Featured here at the annual meeting of the American Chemical Society, the vaccine of the company, called RotaShield, should be on the market by the middle of next year.

Hsieh announced that clinical trials involving 10,500 children in nine countries showed that RotaShield limit the severity of the disease in 80% to 95% of cases. The vaccine is composed of human viral proteins inserted in a similar virus affecting rhesus monkeys.

The experts were initially disappointed that prevention is not the strong point of the vaccine, said pediatrician S. Michael Marcy of the Kaiser Foundation Hospital Panorama City, California, a member of the American Academy of committee of Pediatrics infectious diseases. However, he said the new vaccine will be a great improvement over existing treatments, which amount to just give fluids to sick infants. For this reason, Marcy said, "This vaccine is a winner."

Although rotavirus sickens 3.5 million people - mostly infants - in the United States each year, it is the deadliest in developing countries, where access to health care is limited and poor sanitation. It is also common in the southern United States and within the African-American families, says Hsieh. She says Wyeth-Lederle considering recommending the universal oral vaccination for infants at 2, 4 and 6 months of age.

BETHESDA, MARYLAND - Nobel Laureate David Baltimore Price challenged a fundamental principle of research AIDS: a type of immune cell is regularly able to seek and destroy cells infected with HIV. Speaking yesterday at the Ninth Annual Conference on progress in the development of vaccines against AIDS, Baltimore, virologist at the Massachusetts Institute of Technology (MIT) and the head of a National Institutes of vaccine advisory committee health against AIDS, suggested that HIV effectively disarm the immune cells, white blood cells called cytotoxic T lymphocytes (CTL). The findings may shed light on why some experimental vaccines work in monkeys.

A crucial problem in the vaccine work against AIDS is to determine which immune responses to a vaccine must stimulate. Many researchers focused on antibodies, which GLOM the virus in the blood and help mount a successful infection. Much attention was also paid to CTL, who is like smart bombs, target and destroy cells that HIV has already infected. But the laboratory Baltimore has cast doubt on CTL can do the job themselves

Baltimore and Kathleen Collins MIT CTL guru Bruce Walker of Massachusetts General Hospital, started with two deceptively simple questions :. CTL can actually kill cells infected with HIV? Or to the target cells, such as those infected with cytomegalovirus and other pathogens, produce a factor that protects against CTL? To answer these questions, researchers have developed a test to gauge whether HIV interferes with the production of CTLs. For the immune system to produce CTL against specific pathogens, an infected cell must hold pieces of the pathogen on its surface, spreading what the enemy looks like. The Baltimore team found, however, that an HIV protein called NEF prevents infected cells display fragments of HIV to the CTL-part of the immune system, essentially blindfolding it.

"It seems very interesting," said Anthony Fauci, head of the National Institute of Allergy and Infectious Diseases, the meeting of the sponsor. "We need to take a step further and see up where you can push it. " Baltimore emphasizes that it is impossible to extrapolate from test-tube results to people. But he said the study may help explain why apes and humans infected with HIV that lack NEF gene appear to be unharmed by the virus: Maybe the infected cells stimulate the production of anti-HIV CTL antibody which butterfly infection early on.

- Scientists have genetically Alzheimer's a new strain of mice that can be a model of the early stages of Alzheimer's disease. Even before the brains of human patients develop a characteristic of the disease - the clusters of proteins called plaques - their memories are deteriorating and they lose neurons. The new mice, described in tomorrow's issue Nature , also show neurons and memory loss without plaques, suggesting they could provide a testing ground for drugs intended to slow the progression of the disease in humans. But all the experts are not convinced that the team created an accurate model for early Alzheimer's disease.

In recent years, plaques, which accumulate over time from sticky protein, called insoluble amyloid, became the first suspect to cause the debilitating symptoms of Alzheimer's disease . But some researchers have come to suspect that another protein, produced as an intermediate step when cells chop a long molecule called amyloid precursor protein (APP) to form amyloid could injure neurons before scar plates the brain. test tube studies, for example, suggested that the APP fragment is toxic to neurons.

Now Jo Nalbantoglu, a molecular biologist at McGill University in Montreal and colleagues created mice that have brains that are riddled with these precursor fragments. To do this, they added that the part of the APP gene for amyloid precursor mouse embryos. When they grew into adults, the experimental group had much more trouble remembering how to solve a maze that made the mice in a control group.

Researchers then dissected the brains to see why. When they electrically stimulated living slices of the hippocampus, a memory center for the signal persisted in neural pathways known for 0 minutes in the control mice, but died after about 15 minutes in mice with large amounts of amyloid precursor fragment. In addition, 18-month-old experimental mice had a lower density of 20% of the neurons in the CA1 region of the hippocampus - an effect observed in human Alzheimer's patients. Previous mouse models, however, have failed to show that death characteristic of nerve cells.

neuroscientist Mark Mattson of the University of Kentucky, Lexington, called the work "important progress." But Sangram Sisodia Johns Hopkins University School of Medicine, who is working on mouse models of Alzheimer ' Alzheimer others think neuronal loss could be an artifact of how the Canadian team had neurons to be a true Alzheimer model mice are going to produce amyloid plaques and develop -. and they show no biochemical evidence either. then Nalbantoglu plans to seek these plaques in aged mice while investigating how the precursor proteins could be the cause of memory loss.

PARIS - A common virus may help the AIDS virus to infect certain types of cells and wreak havoc on the immune system. The results, reported in tomorrow's issue of Science * require closer symbiotic relationship between HIV and its possible ally - Cytomegalovirus (CMV) -. Imagined before

CMV, a member of the herpesvirus family that infects 80% of adults and almost all HIV-infected homosexual men, has long been a prime suspect as a cofactor AIDS. A team led by Marc Alizon at the Cochin Institute in Paris, in collaboration with Michel Seman at the University of Paris, began probing whether HIV can use a protein called CMV US28 to enter into certain types of cells. The protein is expressed in cells experimentally infected with CMV. US28 had previously been shown to act as a reception point, or receptor, for the same immune system molecules called chemokines that bind to CCR5, a receptor used by HIV strains which dominates during the early stages of signaling infection.

In determining whether US28 could act as HIV accomplice, the French group has inserted the US28 gene in a human cell line that HIV normally do not infect. The group then sets Alizon those cells that express the protein US28 on their surfaces, various strains of HIV. In these and related experiments, the team found that Alizon US28 bearing cells were easily infected with HIV strains that normally use the CCR5 receptor on human chemokine, and a little less easily by strains that use another human receptor, CXCR4.

"the results are provocative and potentially important for HIV pathogenesis," says Philip Murphy, a chemokine receptor expert at the National Institute of Allergy and Infectious Diseases in Bethesda, Maryland. Adds David Posnett immunologist at Cornell University Medical College in New York who has studied CMV: "I wonder what it all means in real life."

Indeed, it is not yet clear if the French group results, which are limited to cell lines laboratory are relevant to people with HIV. "There is a total lack of information about when, where, and how many US28 is expressed in people infected with CMV," Murphy said. So experts continue to debate whether CMV is simply an opportunistic organism enjoying the immune suppression caused by HIV, or a partner in the destruction of the immune system.

* For details, Science Online Subscribers can create a link to the full report.

infectious disease researchers are hoping to return to the Democratic Republic of the Congo soon to try to trace an exotic infection is alarming experts public health: the largest outbreak ever observed in humans of a virus called monkeypox well known. A first cousin of smallpox, once feared, monkeypox causes almost identical symptoms.

According to a Research News in tomorrow's issue of Science * between February 1996 and February 1997 at least 92 cases of the disease and three deaths were reported in remote area of ​​what was then Zaire. Only 37 documented cases were reported from 1981 to 1986. These results led to in-depth discussions on what could be the cause of the epidemic -. In particular, if the virus moves from man to man more easily than before

medical epidemiologist Ali Khan Centers for Disease Control and Prevention (CDC) in Atlanta led an international team, organized by the Organization World health (wHO) and the Zairian Ministry of health, who visited 12 villages in the center of the epidemic of five days in February, cutting short his trip due to civil unrest. As Khan and his colleagues detailed in Morbidity and Mortality Weekly Report from the CDC ( MMWR ) April 11, they believe 73% of 89 people they studied were infected with d 'other people. It would be a big jump from "secondary contact" rate of 30% reported by epidemiologist and expert monkeypox Czechoslovak Zdenek Jezek, who was from 1981 to 1986 studies in Zaire. The recent survey also found a patient who seems to have been the source of eight other infections, which is twice the highest chain of transmission observed previously. "This is not only an outbreak of a rare exotic disease in the middle of nowhere," Khan said. ". Personally, I am concerned about what would happen if the disease manifests itself in a big city"

an explanation of the epidemic, launched by Jezek and others, is that vaccination against smallpox - which also confer immunity to monkeypox - were so successful that they were arrested there almost 2 decades, creating an ever-increasing pool of people who are sensitive to animal viruses. Immunity is further compromised because the Democratic Republic of Congo has high rates of HIV infection, which paralyzes the immune system. Civil war may have contributed another factor: Faced with a growing threat of famine because of the unrest, villagers may have increased their hunting animals that carry monkeypox, which include monkeys, squirrels and rats

In. virologist Peter Jahrling of the Medical Research Institute of the US Army Infectious Diseases at Fort Detrick, Maryland, "low probability" that the epidemic spreads further. "But it is not zero," he added. To get closer, WHO hopes to organize another mission in a month if the political situation is relatively calm. Khan is eager to return. "It is important to go back there and ask what is the extent of the disease and how transmission occurs," said Khan. "We are all waiting for better data."

* For details, Science Online subscribers can link to the full text of the news story about the search.

A strain of bacteria causing the plague that is resistant to antibiotics normally used to treat the disease occurred in Madagascar. Although researchers have isolated it say they know of no other instances of resistant bacteria, they note that genes that confer drug resistance can easily spread to other plague strains, which pose a threat new pandemics of disease.

Transmitted primarily by flea bites, the last bubonic plague broke out as a pandemic, there are more than 100 years in Hong Kong before spreading around the world. Today, although the disease is always fatal if not treated in time, antibiotics have reduced mortality in patients with fever of about 10%.

But tomorrow New England Journal of Medicine , a team of researchers from the Institut Pasteur in Paris and Antananarivo, Madagascar, reports having isolated a drug-resistant strain of Yersinia pestis , the bacterium responsible for plague, a patient in Madagascar. The patient has not responded to conventional therapy of the disease, a cocktail of antibiotics chloramphenicol, streptomycin and tetracycline. Y. pestis isolated patient also failed to respond to another antibiotic mixture containing sulfonamides and tetracycline, which is often given to people who may have been exposed to plague. The patient survived, however, thanks to another antibiotic, trimethoprim, which the virus strain was not resistant.

Just how the bacterium manages to outsmart the drugs are not yet clear. But researchers report the isolation of the new strain of a small circular DNA strand, known as a plasmid. Similar plasmids carry the genes for resistance to an antibiotic with other resistant bacteria such as Enterobacteriaceae and E. coli inhabiting the intestines of humans and other animals. The team showed that in the test tube plasmid could be transferred to the resistant Y. pestis both a laboratory strain of the bacterium E. coli . "The transfer [of plasmids] occurs at a high frequency," said team member Elisabeth Carniel of the Institut Pasteur in Paris, suggesting that antibiotic resistance could easily spread.

David Dennis of the Centers for Disease Control and prevention in Fort Collins, Colorado, cautions that this discovery could have international implications, "it is an isolated case, but it seems a warning that we must be alert to the possibility that it could spread to other strains, "he said. "If it does, it would be a significant public health problem."

One of the keys to a long life is to eat less - at least for laboratory rats and fruit flies. Now a study of primates, published in this month of American Journal of Physiology suggests that reducing caloric intake to 30% below the level regarded as normal may benefit the heart. Rhesus monkeys on the low-calorie diet have higher levels of cholesterol and triglycerides lowest levels of 'good', the two that guard against heart disease and stroke in humans. The advantage is greater for young people of middle-aged monkeys and shrinks in old age.

For the last decade, molecular biologist George Roth of the National Institute on Aging has been studying the effects of calorie restriction on rhesus monkeys. All 60 monkeys given the same diet, but half are only allowed 70% of the calories normally consumed as a monkey. In previous research, Roth and colleagues have slightly lower blood pressure, improved glucose tolerance and insulin sensitivity (which means that the animals are less likely to develop diabetes), and lower body temperatures in the low-cal group. "What we think is that animals that are restricted are shifting their metabolic strategy of growth and reproduction in a life care strategy," said Roth.

In this document, Roth announcement of results relative to compounds surveillance levels that influence cardiovascular health. the monkeys who ate less had higher levels of normal HDL2B, a type of high-density lipoproteins and protective cholesterol. the largest increase (83%) was for the youngest group of monkeys - 10 years - and the least (16%) for older monkeys, until the age of 28. the levels of people of old age means. about 13 to 15 years in triglycerides were 41% lower than the monkeys on the full meal plan calories. juvenile levels were 11% below normal, and levels were 8% higher than normal for the older monkeys.

"There is solid information," said Richard Weindruch, a gerontologist at the University of Wisconsin, Madison. The next step, says endocrinologist William Cefalu of Bowman Gray School of Medicine in Winston-Salem, North Carolina, is to relate the results to disease. Indeed, the monkeys will soon be tested to determine if they develop heart disease and to what degree, Roth said.

Potent cocktails of anti-HIV drugs can fight the AIDS virus to undetectable levels in the blood. But a pair of tomorrow's paper Science (pp. 1291 and 1295), report that the virus can survive the bombing in a small number of T cells, immune cells that are the main HIV target. Viruses in this hidden reservoir, moreover, can be awakened from their shock shell and allowed to reproduce, at least in the test tube. Or current treatment regimens can take many years to completely rid the body of HIV, experts say, or they are not powerful enough to do it

Although HIV had already been taken lurking in cells Immunity after medical treatment, some scientists had speculated that the virus might exist in a damaged form of impotence. To check this perspective, two research teams - one led by immunologist Robert Siliciano at Johns Hopkins University School of Medicine in Baltimore, and the other by virologist Douglas Richman of the University of California, San Diego, School of Medicine in La Jolla --looked for HIV in the so-called memory T cells, which help lead the attack when the immune system encounters microbial invaders it has seen before.

researchers took blood cells, including memory T cells, HIV-positive patients who were on a strict diet of multi-drug therapy and cultured with cells from people not infected. When the researchers triggered the memory T cells become activated, the virus began to replicate and infect HIV-negative cells - even if viral levels in HIV-infected cells were tiny. Although the results seem to confirm that HIV survives an attack of chemotherapy, the researchers did find some good news. There was no evidence that the virus had mutated survivor, suggesting that it had not become drug resistant

AIDS researchers are not surprised by the viral return. "We knew that the patients during this time period become positive virus if treatment is withdrawn," said retrovirologist John Coffin of Tufts University in Medford, Massachusetts. "The virus still has to be somewhere." Indeed, the results "should not have any impact on what we recommend to patients," said Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases in Bethesda, Md. "We are reaping huge benefits for patients bearing the virus as low as possible for as long as possible. "

Like a captain on a shoot a rocket to call for help sinking ship, distressed arteries attract immune cells. But instead of saving the arteries, immune cells appear to accelerate their decline. The findings, reported in today's issue of Journal of Clinical Investigation , suggest that put a damper on some of this distress call may be a new way to treat heart disease.

Everyone knows that "bad" cholesterol tends to accumulate in the arteries and often leads to atherosclerosis. But for many other risk factors - such as cigarette smoke and certain bacterial infections - the cause of the disease mechanism is unclear. One thing these risk factors have in common, however, is that they trigger an inflammatory response and repair, said Robert Terkeltaub Hospital of the Veteran Administration in San Diego. We knew that the precursor macrophages - wandering cells made by the immune system to consume bacteria and dead cells - accelerates the deposition of fat in the arteries bruised

Terkeltaub enlisted colleagues at Scripps Research Institute La Jolla. In California, and the University of California, San Diego, to try to understand how these precursors called monocytes could be attracted to the injury. Working on mice, Linda Curtiss Scripps transplanted bone marrow that churn white blood cells, with or without the mouse version of CXCR-2, a receptor for chemokines - the distress call from the injured cells to the lesion . The team fed two groups of mice a diet of artery hardening ". And a milkshake over it" the equivalent of one hamburger per day, Terkeltaub said, After 4 months, the mice with the receptor exhibited arterial lesions 2.5 times the size of lesions in mice lacking the receptor; the CXCR-2 mice also had significantly higher macrophage account.

The discovery shows that the modification of the immune response can change the course of atherosclerosis, said Alan Greater Columbia University. The implication, he said, is that compounds that block chemokine receptors could someday be used to protect people injured arteries.