Health Meaning

A committee convened by the Institute of Medicine (IOM) proposed a new name for a condition known variously as chronic fatigue syndrome or myalgic encephalomyelitis. The new name unwieldy: systemic disease effort intolerance, or Minion. In a report published today, the committee also suggests a new set of diagnostic criteria for Minion.

Having reviewed more than 9,000 scientific studies, hear expert testimony, and solicit public comments, the Committee concluded that "the name " Chronic fatigue syndrome has done a disservice to many patients, "calling it" stigmatizing and trivializing. " myalgic encephalomyelitis (ME), they noted, "does not accurately describes the main features of the disease."

There are at least 20 sets of diagnostic criteria, the Committee noted that confused patients, clinicians and their families and researchers studying the disease. The proposed diagnostic criteria are more focused on "core symptoms" as a reduced capacity or with disabilities to work and study, malaise after exercise, and sleep "unrefreshing". The report, "Fatigue Syndrome Beyond Myalgic Encephalitis / chronic: Redefining disease," runs 235 pages

Peter Rowe, who heads the chronic fatigue clinic the. S Johns Hopkins Children Center in Baltimore, Maryland, and was one of 15 members, had praise for the process and product. "This report is phenomenal," said Rowe, noting that it had unanimous support. "It has the best summary of the evidence that I have ever read." The US Department of Health and Human Services and the 'social security administration sponsored the study and the IOM report.

systemic intolerance disease effort does not exactly roll on the tongue. Committee member of the IOM Ronald Davis, a biochemist who heads the genome center at Stanford University in Palo Alto, California, said the group considered some 100 options. "Boy, did we struggle with that," he said. "it is difficult to find a good name, and I do not think it's a perfect name. "

But Davis believes that its essential to eliminate chronic fatigue syndrome. "My son is sick, and when I tell people, they say, 'I had that once, because they were tired once," he said. "ME is a better name, but n 'there is no real data that match the name. "

Davis hopes the report will convince all clinicians they can diagnose the disease and it is real." I will hope get rid of those who can not believe, "said Davis. "They're going to keep it for themselves. It is the incompetence and it is malpractice."

The new diagnostic criteria are based on the so-called consensus criteria in Canada to first put forward in 03. But the report offers a simple separate definition that focuses on "the central element of this disorder," said President Ellen Wright Clayton of the committee to "public dissemination event" held at IOM this morning. "The essence of this disorder is that if patients with this disorder are involved in the effort - cognitive, emotional, physical, whatever - that their symptoms are made much worse and often for an extended period of time, "said Clayton, professor of law at Vanderbilt University in Nashville. the name, she said, is a reflection." We want to name what it is, " she says. "This is what the patient experience."

The committee was "struck by the relative scarcity of research" that disappeared in Minion. "Remarkably little research funding has been made available to study the etiology, pathophysiology and effective treatment of this disease, especially given the number of people affected, "the report said. (He cited estimates say between 836,000 and 2.5 million Americans chronic or ME fatigue syndrome, but Davis points out that some popular diagnostic criteria have definitions too liberal for the condition.)

the report recommends a multidisciplinary committee reviews the diagnostic criteria Minion within 5 years. Rowe said they may want to review the name, too. "We do not think it's going to be the name forever, but it is a step forward," he said.

SEATTLE, WASHINGTON When French scientists presented the results of a drug test at a conference Ebola release Monday, they did it with a lot of warnings, but their message was hopeful: the drug favipiravir seemed to reduce mortality in people with low and medium-high levels of virus in the blood the researchers told reporters at the Conference on retroviruses and opportunistic infections (CROI) here.

But when the head of Denis Malvy study from the University of Bordeaux in France has presented more details on the results CROI, many colleagues have cooled. Many scientists have criticized the evidence and the design of the trial, which is underway at four clinics in Guinea. "It tells us nothing," said epidemiologist Scott Hammer of Columbia University, who chaired the meeting.

In her presentation, Malvy focused on a group of 40 patients who started the trial with viral loads lower than 29 others who obviously do not enjoy favipiravir. As he said on Monday, only six of the 40 patients died than half what was expected on the basis of similar patients treated in the same clinics during the last 3 months. In addition, after 4 days of starting treatment on favipiravir, a drug against influenza, 51% of these patients had low levels of virus in their blood than the standard test could not detect it. "There was a signal that monotherapy favipiravir can reduce the viral load," said Malvy.

Malvy was careful to note the limitations of what he called a "non-comparative proofing" concept study. "the purpose of this test is to provide evidence that will better designed trials," said Malvy. "This type of test does not provide a high level of proof and does not definitively answer a question." Studies are underway in France with blood samples from the same patients will analyze more closely the evolution of Ebola virus levels every day they received treatment. The researchers will also for the first time to determine if the drug has an effect in monkeys, an animal model widely used for Ebola. And the current study may provide more data.

But Hammer said the trial was "a lot of flaws in it, from study design to data interpretation." The immune system naturally drives down viral levels, making it difficult to separate the effects of the drug, he noted. Because the study did not compare treated with untreated people who sought care at the same time he used what is called a "historical" control-Hammer said he could not determine whether these drops in viral levels or providing putative survival are related to favipiravir.

Since the beginning exploded in August, researchers have vigorously debated how to set up studies of drugs and vaccines for Ebola, some randomized controlled studies advocating, in which a group of patients do not receive the drug as the fastest way to get results. Clifford Lane, deputy director at the National Institute of Allergy and Infectious Diseases of the United States, made this point in his presentation at the meeting, but did not single favipiravir the critical study. "As uncontrolled, supposedly compassionate studies fail to clear conclusions, they blur the water to the point that it becomes increasingly difficult to carry out appropriate studies," warned Lane.

Together with Liberian officials, Lane is about to launch a randomized study of an antibody cocktail called ;. zmapp this study does not include a control group in which patients will receive standard care, but not the drug Lane says Guinea and Sierra Leone have so far refused to participate in the study because of ethical concerns not giving the treatment to all participants. (Sierra Leone has shown some support for the design, however, and discussions are continuing.)

Jean-François Delfraissy, which coordinates the response of France Ebola and also heads the HIV / AIDS research program of the country, said he disagreed with Lane and contrasts the argument zmapp tests as planned. "I'm a principal investigator for a long time with randomized controlled trials, and early combination therapy for HIV, they are not required to show the drugs are useful," said Delfraissy, who co-signed an editorial the Lancet which opposed this design for Ebola treatments. "It's hard to have a randomized trial when mortality is 50% or 60%."

Delfraissy does not rule out supporting the official with zmapp modification. "It is an open question," he said, noting that he had discussions with Lane here. Specifically, Delfraissy said if the studies on monkeys and finer analysis of patient samples were positive, perhaps the standard of care should include favipiravir in the control arm in the studies and zmapp other experimental treatments.

Hammer said he understands the perspective of Delfraissy but said, randomized controlled trials have played an important role in the history of the development of drugs against HIV. It highlights a controversial study in 1997, a year after the so-called "triple therapy" has proven itself found that three antiretroviral drugs were better than two. "We proved," said Hammer. "And there was no BS about it later."

A new report on the ethics of Ebola, released today by the US presidential Commission for the study of bioethical issues, takes a nuanced view of questions about the design of the study, the committee does not comment on placebo-controlled studies, but leaves room for other models too well. "test designs should be methodologically rigorous and capable of generating results that are clearly interpretable acceptable to host communities and, wherever possible, to minimize delays to the completion of the research" the report said. "The well-designed controlled trials placebo can meet these conditions, and innovative designs, such as adaptive randomization, should be considered as a way to answer these research objectives."

* Ebola files: science and Science Translational Medicine made a collection of research articles and news about the Ebola virus and the current epidemic available for researchers and the general public.

Researchers hope to recruit 100,000 Pakistanis and Bangladeshis living in East London in one of the first large studies in the long term to explore the links between genetics and health in a poor ethnic community. The study, launched today, is also one of the largest effort yet to find rare individuals who are healthy, despite the absence of a specific gene.

East London is home to many poor immigrants from Pakistan and Bangladesh, and communities suffering from high rates of diseases such as heart disease and diabetes. The study East London Genes & Health will focus on two groups that are left out of most genetic studies, which rely heavily those of Northern European descent. "It is a great opportunity to improve health and the health of the population in East London," said co-leader of the study David van Heel from Queen Mary University of London, who announced study today. the funding of £ 4 million comes from the Wellcome Trust and the Medical Research Council in the United Kingdom.

researchers also hope to gather information on healthy people who have mutations in both copies of a gene that make it non-functional. These rare individuals could shed light on "what happens when parts of the genetic material are not working," says co-study leader Richard Trembath. If the missing gene protects somewhat against the disease, a drug that targets this gene could treat the disease without causing side effects. An example is PCSK9 , a gene found to be missing in a woman "perfect health" in Texas that led to a new class of cholesterol-lowering drugs, notes van Heel.

These "human knockouts" are extremely rare in the general population. But the chances that someone will inherit two knocked-out copies of the same gene were higher in the groups in which relatives often marry, such as the Pakistani and Bangladeshi communities. (This explains why the rare monogenic diseases are more common in these groups, although the study of these diseases are not the purpose of the study is London, it is the subject of another large British study, Genomes project 100,000.) "It's an opportunity for us to better understand the appearance" of knocked-out genes, van Heel said.

investigators plan to spend 4 years to recruit volunteers 16 and older, healthy or ill, from Bangladesh or Pakistan. Participants will give a saliva sample and allow scientists to access their health records. Sanger Institute Wellcome Trust has agreed exomes sequence (DNA encoding the protein) to the first 25,000 participants, hopefully by the end of 2017, van Heel said. The Broad Institute in Cambridge, Massachusetts, will contribute to genomic analysis.

Some participants may be invited in the next two decades to participate in the study of diseases, gene knockout, and how certain genes influence how people respond to medicines. Volunteers will not receive any direct benefit from the study, Trembath admits, but they will have the opportunity "to make a difference to the health of future generations."

Researchers have found a way to deliver genes to activating molecules called transcription factors in specific tissues of a live animal for the first time. The approach that many have written off as too difficult technically prevented form of liver damage in mice, although it has many more technical hurdles before it can be used in other tissues, or in people.

"This is a very exciting job," said Hsiang-Rong Tseng, a chemist at the University of California (UC), Los Angeles. ". It will bring the area of ​​provision of transcription factor in a different place "

Our cells produce over a thousand unique transcription factors, each of which binds to a specific region of DNA to ask the transcription of a gene. created from DNA from an RNA template for a new protein Modification of the activity of these factors could, for example, an amplifier for the production of proteins that suppress tumors or reduce inflammation, and even reprogramming of adult cells in immature cells or types of cells. and unlike other gene therapy approaches that introduce permanently DNA to stimulate the production of proteins, factors transcription decompose and leave no lasting effect on the genome.

But cells have ways to close on or destroy relatively large proteins such as transcription factors when they are delivered to the outside rather than to be realized within the cell, said Niren Murthy, a Bioengineering at UC Berkeley. If a transcription factor enters a cell at all, he will eventually digested in a waste disposal organelle called the lysosome, and never will where it can turn on a core gene. "This remains a major unsolved problem," he said. And from proteins, transcription factors are particularly sensitive to chemical modification, he adds. Linking to useful molecules that might interact with cell receptors or penetrating membranes often means changing their chemical structures so they are no longer their work.

in 2011, the group Tseng has found a new way to deliver bulky transcription factors in cells without substantially altering their structure chemical. by setting a transcription factor to a DNA loop that contains the same sequence, it is intended to recognize in the cell, and then wrapping it in a positively charged nanoparticle that can penetrate the cell membrane, they were able to provide the protein in human cells in a dish.

in the new study, Murthy and his colleagues built on this basic concept connection to attach a transcription factor to a part of the DNA, but they used DNA as scaffolding to hold several other molecules that come in handy on the trip of the transcription factor. This new complex, which they called an assembled DNA recombinant transcription factor (DART) has two chemical chains that can disrupt the membrane of a cell lysosome. They are capped with sugar molecules that prevent them from working until the DART is trapped in the highly acidic contents of the organelle. These sugars also originally intended DART specifically the liver cells by interacting with receptors on their surfaces.

For the first prototype DART, the group chose a well-studied transcription factor called Nrf2, which regulates a number of inflammatory and antioxidant genes. "In animal models, it has literally been able to protect against all known inflammatory diseases, from Alzheimer's disease to liver disease to atherosclerosis," says Murthy. To test the ability of the DART send this protein in the liver, the researchers first injected mice with a high dose of the painkiller acetaminophen pain which is likely to cause liver damage. an hour later, they injected DARTs of Nrf2 bearing.

They found that the DARTs were taken up primarily in the liver and increase the expression of three genes known to protect against oxidative stress. liver samples of treated mice closely resembled DART those of healthy mice, while livers of untreated mice showed significant damage, the group announced online today Nature Materials .

These results are "quite dramatic "said José Manautou, a toxicologist at the University of Connecticut, Storrs, and treatment may be helpful for patients with acetaminophen overdose. But these patients usually arrive at the hospital a day after ingestion, not an hour, he said. Murthy's team is currently working on studies to see if the treatment can actually reverse existing damage, including the effects of chronic liver disease.

Others are much more interested in seeing DARTs work on other tissues. "It is relatively easy to get things made by liver cells," says David Frank, an oncologist at the Dana-Farber Cancer Institute in Boston. "It's always a bit the first step in a new technology delivery. "But he sees significant potential in cancer, for example, if a DART could incorporate a mutated version of a transcription factor that stops the genes that promote tumor growth.

Murthy has no immediate plans to work on targeting other tissues. the sugar they used in this study has a double objective at hand disrupt membranes and liver targeting. "in theory, you could do the same with peptides and antibodies and things like that, "he said," but the chemistry is going to get much more complicated. "

Tseng, who continued to work on its own transcription factor delivery method to reprogram adult cells into stem cells, is enthusiastic about the DART strategy. "We struggled trying to find a good way to apply this transcription factor Delivery of history," he said. "I could not think of anything better at this point." But he warned that the proteins they -Same are very expensive, which puts extra pressure on the use of transcription factor therapies. "If they work well, then I think the cost may not be the issue," he said, "but you need to find the key applications beyond the liver damage. "

The world is facing an epidemic of multidrug-resistant typhoid. This is the conclusion of the largest study to date of the genomes of the bacteria that causes the disease, Salmonella enterica Typhi. According to researchers, a clone of the bacterium that is often multiresistant, called H58, rolls across Asia and Africa. Its spread is likely to increase the cost of treatment and lead to more complications, they warn.

"There is a sense of urgency now," said Gordon Dougan, a geneticist at the Wellcome Trust Sanger Institute in Hinxton, UK, and an author of the paper.

typhoid spread by contaminated water or food, causing fever, headaches and other symptoms. If untreated, the disease can lead to complications such as gastrointestinal perforation and kill up to 20% of patients. estimates range from 10 million to 30 million cases per year. About 0,000 people die. S. enterica Typhi that are resistant to multiple antibiotics appeared in the 1970s but H58 was of particular concern to scientists because it is cropping up in more and more countries.

for an overview of its spread, the scientists analyzed the genomes of 1,832 samples from 21 countries Asia, Africa and Oceania. The clone probably emerged in South Asia around 1985 and then picked up the resistance genes in subsequent years, before spreading to Southeast Asia and Africa, Dougan said.

In Africa, the clone was probably introduced repeatedly in Kenya and was broadcast from there to the south, the authors report online today in Nature Genetics . In an article last month in PLOS Neglected Tropical Diseases , Dougan and other scientists followed the emergence of H58 in one hospital in Malawi. From 1998 to 2010, there were an average of 14 typhoid fever diagnoses a year in hospital. Approximately 7% of isolates were resistant to multiple drugs. In 2014, there were 782 diagnoses, 97% with multidrug resistance. "As soon as it arrives in your country, you have to turn to more expensive antimicrobial," said Dougan.

It is not known why H58 is so successful. One possible explanation: The clone may have mutated to survive better in the fabric carriers that spread the disease without becoming ill themselves. There are some genetic changes in H58 that can point to that says Dougan. "But that's speculation," he warns. Why some bacterial clones become dominant is still a mystery, says Mark Achtman, a microbiologist at the University of Warwick in the UK. "It is a phenomenon that we see again and even in different bacteria and it has never been heard. "

The document is one of the largest samples of bacterial genome that whoever published Achtman said. Much was already known about H58 spread, he said. "But this is the first time we had such a comprehensive list of Salmonella typhi and the H58 group in typhi." Said Dougan he and his colleagues have sequenced more typhoid isolates to identify the origins of H58.

Some people enrolled in clinical trials with the US National Institutes of Health (NIH) continue the use of experimental drugs despite the possibility compounds have fungal contamination.

NIH suspended operations yesterday at a plant that makes experimental drugs for clinical center of the body following an investigation by the Food and Drug Administration (FDA) that revealed multiple problems that could expose sterile drugs to contamination. Forty-six trials currently underway receive the materials of the installation, and the NIH is looking for other sources of products for about 250 patients involved in the studies. In some cases, however, find other sources will not be possible, and some tests will be delayed, says Lawrence Tabak, principal deputy director of NIH.

In addition, some test subjects, after being informed of the risks, asked to continue their experimental treatments made by the now closed facility. The Director Francis Collins NIH has granted exceptions to those whose conditions could be severely compromised if they receive their next scheduled dose. They will be monitored for signs of infection. "Many of them have taken products for some time, without adverse effects. The risk of infection is low, but we still want to be careful," said Tabak.

"This is a painful and unacceptable situation," Collins said in a statement. "the fact that patients may have been put at risk due to non-compliance with standard operating procedures in the Development section pharmaceutical NIH clinical Center is deeply troubling. I will personally supervise the measures necessary to protect patient safety and to remedy the position as soon as possible. "

In April, an employee of Clinical Center had noticed what appeared to be a fungal infection in a vial of albumin used in the administration of interleukin drugs in experimental-after studies was unable to get the liquid out of the bottle. visual inspection of about 650 bottles of the same batch has revealed additional contaminated vial. Six patients from three studies were given bottles of the same lot, although it is unclear if these bottles or others were infected. At this point, none of the six have developed signs of infection or disease.

After the episode in April, an internal review was conducted, says Tabak, who noted several problems with the physical installation. Although the exact date is unknown, at some point the FDA received an anonymous complaint and conducted an unannounced inspection of the facility located on the NIH Bethesda, Maryland, campus between May 19 and May 29. Their 14-page assessment identifies a number of shortcomings, both physical and operational. An exhaust duct leading from one of the "clean rooms" of the installation on the roof was missing a filter or screen, for example, and flaws in the air handling system could expose the sterile products microbial contamination during processing. The report noted deficiencies in the processes of cleaning and disinfection (insects were found in two of the five cleanroom ceiling light berries), and examples of the formation of apparently insufficient staff (laboratory workers with clothes that have left part of their face, neck and arms exposed).

to date, all the facility's products were visually inspected, and no obvious additional contamination was observed. NIH is attempting to send products to a contracting laboratory outside of further testing, which could take several weeks. They are also in the process of contacting and monitoring of patients in the 43 remaining studies. Treatment studies for autoimmune diseases and rare genetic as well as various forms of cancer are among those likely to be affected.

A full review with external experts in engineering, microbial practices, and sterility practices is expected, and the NIH is intended to provide a temporary corrective action plan to the FDA on 19 June.

In the fall of 2013, the emails arrived in scientists from dozens of inboxes informing that their work had been selected for the examination of a project to replicate 50 high-impact papers cancer biology. The project Reproducibility: cancer biology, an open ambitious scientific effort to check whether the key results in the best journals can be replicated by independent laboratories, has raised concerns in the community. Almost all scientists targeted by the project who spoke with Science agrees that cancer biology studies, as in many other areas, too often turn be irreproducible. But few feel comfortable with this particular effort, which plans to announce its conclusions in the coming months. The leaders of the project say it will ultimately benefit the field by measuring the magnitude of the problem of reproducibility in cancer biology.

To read the full article, see the June issue 26 Science .

Vaccines save millions of lives each year by teaching the immune system how to fight against certain viruses or bacteria. But a new study suggests that, paradoxically, they could sometimes teach the pathogens become more dangerous too.

The study is controversial. It was made in chickens, and some scientists say there is little interest for human vaccination; they fear it will strengthen doubts about the appropriateness or safety of vaccines. It should not, says lead author Andrew Read, a biologist at Pennsylvania State University, University Park: The study provides no support for the anti-vaccine movement. But it suggests that some vaccines may be monitored more closely, he argues, or supported with additional measures to prevent unintended consequences.

evolutionary science suggests that many pathogens are not life threatening or even not very virulent, because if they kill their host too quickly that they can not spread to other victims. Now enter the vaccination. Some vaccines do not prevent infection, but they do reduce how sick patients become. As supported Read the first time in a document Nature 14 years ago, keeping alive their guests as "imperfect" or "leaks" could give vaccines deadly pathogens from one side, it allowing them to spread when they would normally burn quickly.

now, Read has published a paper showing that what seems to have happened with Marek's disease, a viral infection in chickens. Marek's disease is spread when infected birds shed virus from their feather follicles, which is then inhaled dust by other chickens. Poultry farmers to vaccinate against the disease, maintaining their healthy flocks but keeps chickens from becoming infected and spreading the virus regularly. In recent decades, Marek's disease has become much more virulent that some scholars believe is the result of vaccination.

Read chickens and researchers from Pirbright Institute in Compton, UK, infected with Marek's disease virus of different strains known to cover the spectrum of low to high virulence. When birds are not vaccinated, infection by highly virulent strains killed them so fast that they lose very little virus-orders of magnitude less than when they were infected with less virulent strains. But in vaccinated birds, the opposite was true: People infected with the more virulent strains of virus shed more than birds infected with less virulent strain

In one experiment unvaccinated birds infected the most virulent strains were housed together. with healthy birds. Again, the infected chickens had died in a short time, leaving no chance of spreading the disease to their healthy cage mates. But when the vaccinated birds were infected with the highly virulent strain, they lived longer and all healthy birds housed with them became infected and died. So "immunization allowed the onward transmission of the virus otherwise too deadly for transmitting, unvaccinated people at risk of severe disease and death," the authors write online today in PLOS Biology .

study is compelling, said Michael Lässig, a physicist at the University of Cologne in Germany, who studies the evolution of flu. "But it is a very special set of circumstances" he warns. "I would be careful to draw general conclusions."

Adrian Hill, a vaccine researcher at the University of Oxford in the UK, said the experiments support the idea that vaccines have made of Marek's disease deadly, but do not prove many other things have changed in the poultry industry in the last decades. flocks became much larger, for example, which could also encourage more virulent strains. But Read said these "hot strains" would disappear very quickly if vaccines were taken

Hill did not doubt that some vaccines may lead to increased virulence. the real issue is the probability to occur. His response: It is very unlikely, and not something we should be worried. "They took 15 years to do an experiment on the only example of what happens."

Read counters that there may be other examples. Feline Calicivirus, which causes a respiratory infection in cats, is a strong candidate, he said, "there have been outbreaks of" superhot Watch is particularly concerned about the bird flu in Europe and the United States, whole poultry flocks are generally slaughtered to stop an epidemic "strains in vaccinated populations." ;. Asian farmers often use birds vaccine against influenza. "You might have the emergence of strains superhot," as a result, they say it. Ab Osterhaus, a virologist at Erasmus MC in Rotterdam, the Netherlands, said it is "very unlikely, but a scenario can not be excluded."

But what about human diseases? Most human vaccines used today are not "leaky"; they are very good at stopping the transmission of the disease. But researchers are turning to diseases that are more difficult to protect against, such as malaria or HIV, they set their sights lower, to vaccines that prevent severe disease, but not infection. "We are entering the era of vaccines fleeing humans," says Read. Candidate vaccines against Ebola and malaria which recently received an important stamp of approval in Europe should certainly be used if they are safe and effective, he said, but could lead to more virulent pathogens. "We need to have a responsible discussion about it."

but for Hill, the comments themselves are irresponsible. Read "no more evidence that this will happen with an Ebola vaccine that will happen with another vaccine in humans," he said. "He should stop scaremongering." The whole distinction between vaccines and fleeing nonleaky is flawed, Hill argues: ". Each vaccine is pierced, in that some people are not protected by it, some people are partially protected, some people have the disease prevention, and other infection prevention not " millions worldwide receive shots of each month and there is no evidence that this has never led to a deadly disease become, said Hill.

moreover, the natural immunity should have the same effect, he adds :. After we recover from illness, we usually end up with a limited "leaky" protection against a pathogen that is not very different from what vaccines reach, said Hill "for malaria, regardless of the fact today vaccine is a drop in the ocean of any immunity which is in Africa of all infections to all people."

hill worried that the reading task will play into the hands of antivaxxers. Read but said that even if a human vaccine is never shown to cause dangerous changes in the pathogen, it would not be a reason not to vaccinate. The most important thing would be to support immunization with other vacuum transmission measurements, such as bed nets against malaria.

Ironically, the increase in virulence, it would be even more important to vaccinate everyone, he said, because that universal vaccination would prevent the most dangerous strains of harming anyone. This is in fact what happened in Marek's disease, Read said. "I think because of these vaccines, the industry has created strains superhot, but the vaccine still works beautifully because it can be delivered to any single vulnerable bird."

* Correction, July 28, 4:07 p.m. :. a quote by Adrian Hill, this story has been corrected