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Science Tuesday - Viruses, Mayans, African Sleeping Sickness, and Autism
Basics: Tiny Specks of Misery, Both Vile and Useful
By NATALIE ANGIER, The New York Times, January 8, 2008
I spent New Year’s Eve with friends and family. A couple of days later, my pathologically healthy mother called to say she’d gotten very sick after the party, like nothing she’d experienced before. She thought it had been a stomach bug. Hey, it’s just like in “The Devil Wears Prada,” I said lightly, the perfect way to jump-start your new diet!
Hardy har. By that afternoon, my husband and I had been drafted into the same violent weight-loss program, and for the next 18 hours would treat the mucosal lining of our stomachs like so much pulp in a pumpkin, while our poor daughter ran around scrubbing her hands and every surface in sight as she sought to stay healthy. I am relieved to report that she succeeded, and that her parents lost 10 pounds between them.
The agent of our misery was a virus, very likely a type of norovirus. Named for Norwalk, Ohio, the site of a severe outbreak of vomiting, nausea and diarrhea among schoolchildren in the late 1960s, the norovirus is a small, spherical, highly contagious virus that targets the digestive system. Its sour suite of symptoms is often referred to as “stomach flu,” but norovirus infection is distinct from the flu, which is caused by the influenza virus and targets not the gut but the lungs.
Well, not that distinct. Noroviruses, flu viruses, the rhino and corona viruses that cause the common cold, the herpes virus that causes the cold sore, all are active players in the wheezing ambient pleurisy of January.
As viruses, all of them are, by definition, infectious parasitic agents tiny enough to pass through a microfilter that would trap bacteria and other microbes, tiny enough to fit millions on board a single fleck of spit. All viruses have at their core compact genetic instructions for making more viruses, some of the booklets written in DNA, others in the related nucleic language of RNA. Our cells have the means to read either code, whether they ought to or not. Encasing the terse viral genomes are capsids, protective coats constructed of interlocking protein modules and decorated with some sort of docking device, a pleat of just the right shape to infiltrate a particular cell. Rhinoviruses dock onto receptors projecting from the cells of our nasal passages, while hepatitis viruses are shaped to exploit portholes on liver cells.
Their ergonomic specificity stems from the competition for a niche in a virus-packed world. Viruses very likely arose along with or possibly just before the appearance of the first living cells, nearly four billion years ago, and they have been jimmying cellular locks ever since. “Viruses are found everywhere, in every tree of life,” said Phillip A. Sharp of the Center for Cancer Research at M.I.T., “and every virus has to have a scheme.”
It’s easy to hate viruses for those freeloading schemes: nice trick, forcing me to throw up just so you can get out and mingle. How about if I name an entire class of computer problems after you? Yet viruses can seem almost tragic. Many strains, it turns out, are surprisingly delicate.
“Microbes like the anthrax bacterium can remain dormant in the soil for years” and still retain their power to kill, said Marlene Zuk, author of “Riddled With Life” and a professor of biology at the University of California, Riverside. “But viruses are really fragile, and they can’t survive outside their host for very long.” A few hours, maybe a couple of days left unclaimed on a cup or keyboard, and the average viral spore falls apart.
And they are so nakedly needy. They depend on our cells to manufacture every detail of their offspring, to print up new copies of the core instruction booklets, to fabricate the capsid jackets and to deliver those geometrically tidy newborn virions to fresh host shores. Through us, viruses can transcend mere chemistry and lay claim to biology. Many scientists view viruses, with their lack of autonomous means of metabolism or reproduction, as straddling the border between life and nonlife. But if there is ever a case to be made for the liveliness of viruses, it is when they are replicating and mutating and evolving inside us.
Yet viruses have not only taken; they have also repaid us in ways we are just beginning to tally. “Viral elements are a large part of the genetic material of almost all organisms,” said Dr. Sharp, who won a Nobel Prize for elucidating details of our genetic code. Base for nucleic base, he said, “we humans are well over 50 percent viral.”
Scientists initially dismissed the viral elements in our chromosomes as so much tagalong “junk DNA.” But more recently some researchers have proposed that higher organisms have in fact co-opted viral genes and reworked them into the source code for major biological innovations, according to Luis P. Villarreal, director of the Center for Virus Research at the University of California, Irvine.
Some genes involved in the growth of the mammalian placenta, for example, have a distinctly viral character, as do genes underlying the recombinant powers of our adaptive immune system — precisely the part that helps us fight off viruses.
In fact, it may well have been through taking genomic tips from our viral tormentors that we became so adept at keeping them at bay.
“Our bodies spontaneously recover from viruses more so than overwhelming bacterial infections,” said Anthony S. Fauci, director of the National Institute of Allergy and Infectious Diseases. “Viral infections have shaped the nature of the human immune system, and we have adapted to mount a very effective response against most of the viruses that we confront.” Vaccines accentuate this facility, he added, which is why vaccination programs have been most successful in preventing viral diseases.
Should prevention elude you, well, you may at least lose some weight.
Ancient Yucatán Soils Point to Maya Market, and Market Economy
By JOHN NOBLE WILFORD, The New York Times, January 8, 2008
Scientists using improved methods of analyzing the chemistry of ancient soils have detected where a large marketplace stood 1,500 years ago in a Maya city on the Yucatán Peninsula of Mexico.
The findings, archaeologists say, are some of the first strong evidence that the ancient Maya civilization, at least in places and at certain times, had a market economy similar in some respects to societies today. The conventional view has been that food and other goods in Maya cities were distributed through taxation and tributes controlled by the ruling class.
Bruce H. Dahlin, an archaeologist at Shepherd University in Shepherdstown, W. Va., said in a telephone interview that the new research “introduces some hard-core empirical evidence for a market economy,” adding that the soil studies provide “the first way of confirming that an area that looks like a marketplace is a marketplace.”
Dr. Dahlin was the lead author of a report on the discovery in the current issue of the journal Latin American Antiquity. Richard E. Terry, who conducted the tests, is a soil biochemist at Brigham Young University and an expert in the analysis of soils at archaeological sites.
Archaeologists suspected that a wide clearing at the center of the ruins of Chunchucmil might have been a market, not a ritual plaza. Rock alignments peeking above the surface seemed to outline the positions of stalls and regular pathways; the rock patterns for stalls were too small to be house foundations.
Other research in recent years indicated that the city appeared to have been an important trade center in northwestern Yucatán, connected by a canal to the Gulf of Mexico, 15 miles away. It was doubtful, experts say, that the nearby agriculture could have supported the estimated population of up to 45,000 at the city’s peak around A.D. 500. Archaeologists surmised that the city traded in goods and services for food at an outdoor market.
Dr. Terry’s team took several hundred samples of soil from the clearing and adjacent areas. Food and other organic matter might decay, but they leave chemical traces that survive in the soil. All food materials contain phosphorus, a particularly durable marker of food from long ago.
The researchers applied a dilute acid to the samples and filtered the resulting solution. Exposed to a light from a portable laboratory, the phosphorus in the soil emitted a blue glow; the bluer it was, the greater the amount of the residual chemical. Most samples from the site showed phosphorus concentrations 40 times higher than in surrounding soils, which Dr. Terry said was consistent with results from modern open-air markets in the region.
Stephen D. Houston, a Maya scholar at Brown University who was not associated with the project, said the research was “intriguing work by specialists with a long and distinguished track record in the soil chemistry of Maya ruins.”
Noting that he had been a skeptic of an ancient Maya market economy, Dr. Houston wrote in an e-mail message, “I’m definitely coming around to a belief in these market facilities,” citing suggestive discoveries at other ruins in Mexico and Guatemala.
But Dr. Houston questioned how widespread the market economy was in time and geography. He contended that in most cases, Maya rulers had controlled food distribution through a tax and tribute economy.
Jump-Start on Slow Trek to Treatment for a Disease
By DONALD G. McNEIL Jr., The New York Times, January 8, 2008
Last month, the Bill and Melinda Gates Foundation donated $19 million to the Drugs for Neglected Diseases Initiative to further one of its goals: finding a new drug for African sleeping sickness.
Not that $19 million will come close to doing that. Even if a miracle cure is found, it will take lab work and clinical trials that could easily cost $100 million to prove it is really a miracle and not the Vioxx of the African savannah.
But the gift spotlights just how tricky the search for new treatments can be when the disease is fearsome but nearly forgotten because its victims are poor and obscure.
The plan for sleeping sickness is a series of incremental steps, said Dr. Bernard Pécoul, a former member of Doctors Without Borders who founded the partnership in 2003.
A drug started from scratch might not be ready till 2020 or later. A perfect one, he said, would be taken orally, would cure the disease in less than a week and would have no horrible side effects. But until then, even slight advances in treatment will benefit victims, who now face choices familiar to cancer patients: the cure is so rough that the only thing worse is no cure.
“Sleeping sickness” is too benign a nickname for human African trypanosomiasis, which is caused by a protozoan spread by biting tsetse flies. When the parasites enter the brain, victims hallucinate wildly. They have been known to chase neighbors with machetes, throw themselves into latrines and scream with pain at the touch of water. Only at the end do they lapse into a lassitude so great that they cannot eat, followed by coma and death.
About 150,000 people contract the disease each year, but 50 million people in 36 countries live in areas where they are at risk.
The best treatment now is eflornithine, sometimes called the resurrection drug because it can pull the dying out of comas.
It is almost a miracle that eflornithine is available. It was discovered in 1980 at Pace University in New York. By early 2000, the last 7,500 doses in the world were running out. The patentholder, a precursor of the drug maker Sanofi-Aventis, abandoned it in 1995 because it had not lived up to its anticancer potential. Then, in late 2000, plans to make a topical form emerged. It was the key ingredient in Vaniqa, a cream to prevent facial hair in women.
After critics accused Sanofi-Aventis of catering to vain rich women while letting poor Africans die, the company agreed to make an injectable form of the drug and now gives it free to the World Health Organization and Doctors Without Borders.
But in rural Africa, eflornithine is very hard to use. Patients need intravenous infusions four times a day for two weeks. When a “hospital” is a row of iron beds under a thatched roof, and the “nursing staff” is mostly relatives of the sick who sleep on the floor, round-the-clock treatment is hard. There might be no night nurse to insert an IV line.
For that reason, many countries do not adopt it. They still use the drug melarsoprol, which, Dr. Pécoul said, “is not effective and sometimes kills.”
Melarsoprol, invented in the 1940s, is essentially arsenic dissolved in propylene glycol, the antifreeze ingredient. It can be given once a day for 10 days, which is easier on nurses. But it kills 5 percent of those who take it and burns survivors’ veins.
Dr. Pécoul hopes to have more countries switch to a mix of seven days of eflornithine twice a day — so that night nurses are not needed — plus seven days of nifurtimox, an oral drug that kills protozoa but is ineffective alone. To do that, he hopes by next year to be able to report favorable results from clinical trials under way at six sites in Uganda, Congo and the Congo Republic, and then persuade the W.H.O. to recommend the regimen.
By 2014, he hopes to have evidence that another drug, fexinidazole, is better. It can be taken orally, and in animal tests it cures even late-stage sleeping sickness in the brain within two weeks. But it has not been tested on humans. Phase 1 trials, small tests of its safety in humans, are to start late this year.
Fexinidazole was developed by the German pharmaceutical company Hoechst, now part of Sanofi-Aventis, and abandoned in the 1980s when the company gave up its tropical disease programs, said Els Torreele, who directs the initiative’s fexinidazole project. It is one of a class of drugs known as azoles, like fluconazole, that work against fungi and may work against cancer.
“We tested 500 different azoles,” Dr. Pécoul said. The advantage of adopting an abandoned drug is that the former patentholder has usually done the chemical analyses, animal studies and, sometimes, early human trials, saving millions of dollars.
The $19 million from the Gates Foundation is not for that, but to begin the hunt for a completely new candidate.
Yves J. Ribeill, founder of Scynexis, a North Carolina drug company that will receive much of the grant, said his chemists would fill legions of tiny test tubes with parasites swimming in calf serum, and legions more with mammalian tissue cells, and dose them all with thousands of molecules from chemical “libraries.” Dr. Pécoul’s group has negotiated deals to use about 20 university and drug company libraries.
After gathering “hits” — compounds that kill parasites but not cells — Scynexis has to work out ways to make them into “leads,” which are versions that are potent, safe and easy to make, and will “last long enough in the blood to have an effect and then disappear,” Dr. Ribeill said.
Then trials begin, first in mice, then in other animals and finally in humans. Each will take years and will need further grants like the latest from the Gates Foundation.
“When you have a lead,” Dr. Pécoul said, “you are still far away from having a drug.”
Study Finds Vaccine Preservative Is Not Linked to Risks of Autism
By THE ASSOCIATED PRESS, The New York Times, January 8, 2008
LOS ANGELES (AP) — Autism cases in California continued to climb even after a mercury-based vaccine preservative that some people blame for the neurological disorder was removed from routine childhood shots, a study has found.
Researchers from the State Public Health Department found that the autism rate in children rose continuously in the study period from 1995 to 2007. The preservative, thimerosal, has not been used in childhood vaccines since 2001, except for some flu shots.
Doctors said that the latest study added to the evidence against a link between thimerosal exposure and the risk of autism and that it should reassure parents that vaccinations do not cause autism. If there was a risk, the doctors said, autism rates should have dropped from 2004 to 2007.
Dr. Daniel Geschwind, a neurologist at the David Geffen School of Medicine at the University of California, Los Angeles, said the focus should be on exploring possible causes of autism, including genetic links.
“Something else must be at play,” said Dr. Geschwind, who had no connection with the study. “And we need to know what that is if we’re really serious about preventing autism.”
The results of the study are in the January issue of The Archives of General Psychiatry. The study did not explore why autism cases increased.
Officials say one in 150 American children have autism, higher than other estimates. Researchers say it is unclear whether the increase stems from changes in classifying autism or whether the increase is actual.
By NATALIE ANGIER, The New York Times, January 8, 2008
I spent New Year’s Eve with friends and family. A couple of days later, my pathologically healthy mother called to say she’d gotten very sick after the party, like nothing she’d experienced before. She thought it had been a stomach bug. Hey, it’s just like in “The Devil Wears Prada,” I said lightly, the perfect way to jump-start your new diet!
Hardy har. By that afternoon, my husband and I had been drafted into the same violent weight-loss program, and for the next 18 hours would treat the mucosal lining of our stomachs like so much pulp in a pumpkin, while our poor daughter ran around scrubbing her hands and every surface in sight as she sought to stay healthy. I am relieved to report that she succeeded, and that her parents lost 10 pounds between them.
The agent of our misery was a virus, very likely a type of norovirus. Named for Norwalk, Ohio, the site of a severe outbreak of vomiting, nausea and diarrhea among schoolchildren in the late 1960s, the norovirus is a small, spherical, highly contagious virus that targets the digestive system. Its sour suite of symptoms is often referred to as “stomach flu,” but norovirus infection is distinct from the flu, which is caused by the influenza virus and targets not the gut but the lungs.
Well, not that distinct. Noroviruses, flu viruses, the rhino and corona viruses that cause the common cold, the herpes virus that causes the cold sore, all are active players in the wheezing ambient pleurisy of January.
As viruses, all of them are, by definition, infectious parasitic agents tiny enough to pass through a microfilter that would trap bacteria and other microbes, tiny enough to fit millions on board a single fleck of spit. All viruses have at their core compact genetic instructions for making more viruses, some of the booklets written in DNA, others in the related nucleic language of RNA. Our cells have the means to read either code, whether they ought to or not. Encasing the terse viral genomes are capsids, protective coats constructed of interlocking protein modules and decorated with some sort of docking device, a pleat of just the right shape to infiltrate a particular cell. Rhinoviruses dock onto receptors projecting from the cells of our nasal passages, while hepatitis viruses are shaped to exploit portholes on liver cells.
Their ergonomic specificity stems from the competition for a niche in a virus-packed world. Viruses very likely arose along with or possibly just before the appearance of the first living cells, nearly four billion years ago, and they have been jimmying cellular locks ever since. “Viruses are found everywhere, in every tree of life,” said Phillip A. Sharp of the Center for Cancer Research at M.I.T., “and every virus has to have a scheme.”
It’s easy to hate viruses for those freeloading schemes: nice trick, forcing me to throw up just so you can get out and mingle. How about if I name an entire class of computer problems after you? Yet viruses can seem almost tragic. Many strains, it turns out, are surprisingly delicate.
“Microbes like the anthrax bacterium can remain dormant in the soil for years” and still retain their power to kill, said Marlene Zuk, author of “Riddled With Life” and a professor of biology at the University of California, Riverside. “But viruses are really fragile, and they can’t survive outside their host for very long.” A few hours, maybe a couple of days left unclaimed on a cup or keyboard, and the average viral spore falls apart.
And they are so nakedly needy. They depend on our cells to manufacture every detail of their offspring, to print up new copies of the core instruction booklets, to fabricate the capsid jackets and to deliver those geometrically tidy newborn virions to fresh host shores. Through us, viruses can transcend mere chemistry and lay claim to biology. Many scientists view viruses, with their lack of autonomous means of metabolism or reproduction, as straddling the border between life and nonlife. But if there is ever a case to be made for the liveliness of viruses, it is when they are replicating and mutating and evolving inside us.
Yet viruses have not only taken; they have also repaid us in ways we are just beginning to tally. “Viral elements are a large part of the genetic material of almost all organisms,” said Dr. Sharp, who won a Nobel Prize for elucidating details of our genetic code. Base for nucleic base, he said, “we humans are well over 50 percent viral.”
Scientists initially dismissed the viral elements in our chromosomes as so much tagalong “junk DNA.” But more recently some researchers have proposed that higher organisms have in fact co-opted viral genes and reworked them into the source code for major biological innovations, according to Luis P. Villarreal, director of the Center for Virus Research at the University of California, Irvine.
Some genes involved in the growth of the mammalian placenta, for example, have a distinctly viral character, as do genes underlying the recombinant powers of our adaptive immune system — precisely the part that helps us fight off viruses.
In fact, it may well have been through taking genomic tips from our viral tormentors that we became so adept at keeping them at bay.
“Our bodies spontaneously recover from viruses more so than overwhelming bacterial infections,” said Anthony S. Fauci, director of the National Institute of Allergy and Infectious Diseases. “Viral infections have shaped the nature of the human immune system, and we have adapted to mount a very effective response against most of the viruses that we confront.” Vaccines accentuate this facility, he added, which is why vaccination programs have been most successful in preventing viral diseases.
Should prevention elude you, well, you may at least lose some weight.
Ancient Yucatán Soils Point to Maya Market, and Market Economy
By JOHN NOBLE WILFORD, The New York Times, January 8, 2008
Scientists using improved methods of analyzing the chemistry of ancient soils have detected where a large marketplace stood 1,500 years ago in a Maya city on the Yucatán Peninsula of Mexico.
The findings, archaeologists say, are some of the first strong evidence that the ancient Maya civilization, at least in places and at certain times, had a market economy similar in some respects to societies today. The conventional view has been that food and other goods in Maya cities were distributed through taxation and tributes controlled by the ruling class.
Bruce H. Dahlin, an archaeologist at Shepherd University in Shepherdstown, W. Va., said in a telephone interview that the new research “introduces some hard-core empirical evidence for a market economy,” adding that the soil studies provide “the first way of confirming that an area that looks like a marketplace is a marketplace.”
Dr. Dahlin was the lead author of a report on the discovery in the current issue of the journal Latin American Antiquity. Richard E. Terry, who conducted the tests, is a soil biochemist at Brigham Young University and an expert in the analysis of soils at archaeological sites.
Archaeologists suspected that a wide clearing at the center of the ruins of Chunchucmil might have been a market, not a ritual plaza. Rock alignments peeking above the surface seemed to outline the positions of stalls and regular pathways; the rock patterns for stalls were too small to be house foundations.
Other research in recent years indicated that the city appeared to have been an important trade center in northwestern Yucatán, connected by a canal to the Gulf of Mexico, 15 miles away. It was doubtful, experts say, that the nearby agriculture could have supported the estimated population of up to 45,000 at the city’s peak around A.D. 500. Archaeologists surmised that the city traded in goods and services for food at an outdoor market.
Dr. Terry’s team took several hundred samples of soil from the clearing and adjacent areas. Food and other organic matter might decay, but they leave chemical traces that survive in the soil. All food materials contain phosphorus, a particularly durable marker of food from long ago.
The researchers applied a dilute acid to the samples and filtered the resulting solution. Exposed to a light from a portable laboratory, the phosphorus in the soil emitted a blue glow; the bluer it was, the greater the amount of the residual chemical. Most samples from the site showed phosphorus concentrations 40 times higher than in surrounding soils, which Dr. Terry said was consistent with results from modern open-air markets in the region.
Stephen D. Houston, a Maya scholar at Brown University who was not associated with the project, said the research was “intriguing work by specialists with a long and distinguished track record in the soil chemistry of Maya ruins.”
Noting that he had been a skeptic of an ancient Maya market economy, Dr. Houston wrote in an e-mail message, “I’m definitely coming around to a belief in these market facilities,” citing suggestive discoveries at other ruins in Mexico and Guatemala.
But Dr. Houston questioned how widespread the market economy was in time and geography. He contended that in most cases, Maya rulers had controlled food distribution through a tax and tribute economy.
Jump-Start on Slow Trek to Treatment for a Disease
By DONALD G. McNEIL Jr., The New York Times, January 8, 2008
Last month, the Bill and Melinda Gates Foundation donated $19 million to the Drugs for Neglected Diseases Initiative to further one of its goals: finding a new drug for African sleeping sickness.
Not that $19 million will come close to doing that. Even if a miracle cure is found, it will take lab work and clinical trials that could easily cost $100 million to prove it is really a miracle and not the Vioxx of the African savannah.
But the gift spotlights just how tricky the search for new treatments can be when the disease is fearsome but nearly forgotten because its victims are poor and obscure.
The plan for sleeping sickness is a series of incremental steps, said Dr. Bernard Pécoul, a former member of Doctors Without Borders who founded the partnership in 2003.
A drug started from scratch might not be ready till 2020 or later. A perfect one, he said, would be taken orally, would cure the disease in less than a week and would have no horrible side effects. But until then, even slight advances in treatment will benefit victims, who now face choices familiar to cancer patients: the cure is so rough that the only thing worse is no cure.
“Sleeping sickness” is too benign a nickname for human African trypanosomiasis, which is caused by a protozoan spread by biting tsetse flies. When the parasites enter the brain, victims hallucinate wildly. They have been known to chase neighbors with machetes, throw themselves into latrines and scream with pain at the touch of water. Only at the end do they lapse into a lassitude so great that they cannot eat, followed by coma and death.
About 150,000 people contract the disease each year, but 50 million people in 36 countries live in areas where they are at risk.
The best treatment now is eflornithine, sometimes called the resurrection drug because it can pull the dying out of comas.
It is almost a miracle that eflornithine is available. It was discovered in 1980 at Pace University in New York. By early 2000, the last 7,500 doses in the world were running out. The patentholder, a precursor of the drug maker Sanofi-Aventis, abandoned it in 1995 because it had not lived up to its anticancer potential. Then, in late 2000, plans to make a topical form emerged. It was the key ingredient in Vaniqa, a cream to prevent facial hair in women.
After critics accused Sanofi-Aventis of catering to vain rich women while letting poor Africans die, the company agreed to make an injectable form of the drug and now gives it free to the World Health Organization and Doctors Without Borders.
But in rural Africa, eflornithine is very hard to use. Patients need intravenous infusions four times a day for two weeks. When a “hospital” is a row of iron beds under a thatched roof, and the “nursing staff” is mostly relatives of the sick who sleep on the floor, round-the-clock treatment is hard. There might be no night nurse to insert an IV line.
For that reason, many countries do not adopt it. They still use the drug melarsoprol, which, Dr. Pécoul said, “is not effective and sometimes kills.”
Melarsoprol, invented in the 1940s, is essentially arsenic dissolved in propylene glycol, the antifreeze ingredient. It can be given once a day for 10 days, which is easier on nurses. But it kills 5 percent of those who take it and burns survivors’ veins.
Dr. Pécoul hopes to have more countries switch to a mix of seven days of eflornithine twice a day — so that night nurses are not needed — plus seven days of nifurtimox, an oral drug that kills protozoa but is ineffective alone. To do that, he hopes by next year to be able to report favorable results from clinical trials under way at six sites in Uganda, Congo and the Congo Republic, and then persuade the W.H.O. to recommend the regimen.
By 2014, he hopes to have evidence that another drug, fexinidazole, is better. It can be taken orally, and in animal tests it cures even late-stage sleeping sickness in the brain within two weeks. But it has not been tested on humans. Phase 1 trials, small tests of its safety in humans, are to start late this year.
Fexinidazole was developed by the German pharmaceutical company Hoechst, now part of Sanofi-Aventis, and abandoned in the 1980s when the company gave up its tropical disease programs, said Els Torreele, who directs the initiative’s fexinidazole project. It is one of a class of drugs known as azoles, like fluconazole, that work against fungi and may work against cancer.
“We tested 500 different azoles,” Dr. Pécoul said. The advantage of adopting an abandoned drug is that the former patentholder has usually done the chemical analyses, animal studies and, sometimes, early human trials, saving millions of dollars.
The $19 million from the Gates Foundation is not for that, but to begin the hunt for a completely new candidate.
Yves J. Ribeill, founder of Scynexis, a North Carolina drug company that will receive much of the grant, said his chemists would fill legions of tiny test tubes with parasites swimming in calf serum, and legions more with mammalian tissue cells, and dose them all with thousands of molecules from chemical “libraries.” Dr. Pécoul’s group has negotiated deals to use about 20 university and drug company libraries.
After gathering “hits” — compounds that kill parasites but not cells — Scynexis has to work out ways to make them into “leads,” which are versions that are potent, safe and easy to make, and will “last long enough in the blood to have an effect and then disappear,” Dr. Ribeill said.
Then trials begin, first in mice, then in other animals and finally in humans. Each will take years and will need further grants like the latest from the Gates Foundation.
“When you have a lead,” Dr. Pécoul said, “you are still far away from having a drug.”
Study Finds Vaccine Preservative Is Not Linked to Risks of Autism
By THE ASSOCIATED PRESS, The New York Times, January 8, 2008
LOS ANGELES (AP) — Autism cases in California continued to climb even after a mercury-based vaccine preservative that some people blame for the neurological disorder was removed from routine childhood shots, a study has found.
Researchers from the State Public Health Department found that the autism rate in children rose continuously in the study period from 1995 to 2007. The preservative, thimerosal, has not been used in childhood vaccines since 2001, except for some flu shots.
Doctors said that the latest study added to the evidence against a link between thimerosal exposure and the risk of autism and that it should reassure parents that vaccinations do not cause autism. If there was a risk, the doctors said, autism rates should have dropped from 2004 to 2007.
Dr. Daniel Geschwind, a neurologist at the David Geffen School of Medicine at the University of California, Los Angeles, said the focus should be on exploring possible causes of autism, including genetic links.
“Something else must be at play,” said Dr. Geschwind, who had no connection with the study. “And we need to know what that is if we’re really serious about preventing autism.”
The results of the study are in the January issue of The Archives of General Psychiatry. The study did not explore why autism cases increased.
Officials say one in 150 American children have autism, higher than other estimates. Researchers say it is unclear whether the increase stems from changes in classifying autism or whether the increase is actual.