A QUANTUM OF SCIENCE
Emergent viral outbreaks show Ebola is not the only "hot zone" virus worth fearing
Sub-Saharan Africa has long been known as the Hot Zone, a place from which some of the world’s most deadly viruses originated. Among them are the well-known Ebola and Marburg viruses, members of the viral hemorrhagic fever (VHF) family that cause extreme fever, internal and external bleeding and rapid death among a frighteningly high percentage of those infected. Other "Old World" (i.e. African) hemorrhagic viral diseases include dengue and yellow fever. Most VHF viruses are carried by rodents – which seem largely immune – and are spread to humans by liquid contact, though some are capable of aerosol infections. (This latter category includes the Marburg virus, which was weaponized by the former Soviet Union in the 1980’s.) Less well-known cousins in this same family are the so-called New World viruses such as hantavirus, as well as the Argentine, Bolivian, and Venezuelan hemorrhagic fevers.
Late last fall an African travel agent was flown from the city of Lusaka to Johannesburg, South Africa, suffering from high fever and external bleeding. She died a few days later. Within the next several days, the paramedic who received her into the hospital, a nurse who cleaned the room following the travel agent’s death, and a nurse who attended the paramedic after he became ill, all perished from the same virus. Another nurse who treated the paramedic was given an antiviral treatment and survived. This was the beginning and end – for now – of an outbreak of the Lujo Virus, named for the two cities where it was first observed (Lusaka and Johannesburg). A member of the VHF family, it has more in common with the New World branch than it does Ebola or Marburg. Genetic analysis by researchers at Columbia University showed that the Lujo virus was a member of the arenaviridae genus (the name comes from the Latin word for sand, referring to the way viral particles of this genus appear when viewed under a microscope). Strangely, arenaviruses are almost unknown in Africa but have several species native to South America. Comparing the genetic sequence of Lujo to other VHF species from Africa showed significant differences, strongly suggesting that Lujo was not a simple mutant or even a more virulent strain caused by reassortment of viral chromosomes (such as is often the case for the influenza virus). Instead, Lujo appears to be the first high-morbidity, high-mortality VHF virus to emerge from Africa’s hot zone in the last thirty years.
In 2006 a paper was published by Dr. C.J. Peters, a member of the University of Texas Medical Branch, discussing the factors that affect the accelerating rate of emergence of new viruses and increasingly deadly outbreaks. He referenced the Emerging Microbial Threats reports issued by the Institute of Medicine in 1992 and updated in 2002, in which all the data pointed to two major factors at play in the increasing danger of deadly microbial outbreaks: multiple ecologic niches and ever-accelerating human travel and transport. In this paper he describes an arenavirus outbreak in a small village in Bolivia in 1962. The village suffered an outbreak of "black typhus" and out of 600 villager there were 107 cases, of which more than four out of ten perished. This is roughly the same morbidity and mortality rates recorded for the medieval scourge of bubonic plague, better known as the Black Death.
Since the 1960's, large sections of the Amazonian plateau have been deforested, and human activity in those regions has reached levels never before seen. The same is true of sub-Saharan Africa, where the Lujo virus emerged in 2008; had the Lujo virus not been caught before it spread thanks to current medical expertise not available in 1962, the "black typhus" outbreak may well have paled in comparison to the devastation Lujo might have wrought.
The story of ecological niches created through human activity has become hauntingly familiar, and authorities predict that the problem will only worsen as population pressures push humans deeper into the hot zones of viral reservoirs in both the Old World and the New.
For more information:
Viral hemorrhagic fever (overview)
Googleblog article on early news of the Lujo outbreak
News article on Columbia researcher’s efforts to analyze Lujo
Genetic Detection and Characterization of Lujo Virus, a New Hemorrhagic Fever–Associated Arenavirus from Southern Africa (Lipkin et al).
NOVA interview discussing Soviet weaponization of Marburg virus
© A Quantum of Science / P. Smalley
Reproduction with attribution is appreciation
Thursday, July 9, 2009
Quantum: the Cute-Baby Effect
A QUANTUM OF SCIENCE
This just in: women like looking at "attractive" babies more than men do. That's unlikely to make any headlines, but the reverse case is where the surprise comes in: if a baby is "unattractive" through some objective standard, women like looking at it *less* than men do.
Researchers at the Clinical Psychopathology Laboratory or McLean Hospital and Harvard Medical School in Boston report that the length of time that women vs. men spent looking at "normal" babies versus those affected by cleft palate, Down's Syndrome or other congenital birth defects were reversed: women spent longer looking at the "normal" babies than men did, but much less time looking at "unattractive" babies than men did. The authors of the study suggest that this might reflect an evolutionary bias on the part of women to spend less time and attention on the less viable of their offspring, correlating subjective lack of aesthetic appeal with decreased potential for viability.
For more information:
Gender Differences in the Motivational Processing of Babies Are Determined by Their Facial Attractiveness (Yamamoto et al.)
© A Quantum of Science / P. Smalley
Reproduction with attribution is appreciation
This just in: women like looking at "attractive" babies more than men do. That's unlikely to make any headlines, but the reverse case is where the surprise comes in: if a baby is "unattractive" through some objective standard, women like looking at it *less* than men do.
Researchers at the Clinical Psychopathology Laboratory or McLean Hospital and Harvard Medical School in Boston report that the length of time that women vs. men spent looking at "normal" babies versus those affected by cleft palate, Down's Syndrome or other congenital birth defects were reversed: women spent longer looking at the "normal" babies than men did, but much less time looking at "unattractive" babies than men did. The authors of the study suggest that this might reflect an evolutionary bias on the part of women to spend less time and attention on the less viable of their offspring, correlating subjective lack of aesthetic appeal with decreased potential for viability.
For more information:
Gender Differences in the Motivational Processing of Babies Are Determined by Their Facial Attractiveness (Yamamoto et al.)
© A Quantum of Science / P. Smalley
Reproduction with attribution is appreciation
Wednesday, July 8, 2009
Food Safety Overhaul: Chickens and Eggs
A QUANTUM OF SCIENCE
Sweeping and ambitious, administration regulations would enact mandatory oversight and tracking of critical foods
Today the Obama administration announced a major overhaul of the US food safety system. Overseen almost entirely by the FDA, some 150,000 individual commercial food producers would be subject to sweeping new regulations that would require traceability for all food and food additives sold in the US. This is a significant increase in the level of government oversight of the food industry and is a response to several high-profile outbreaks of food poisoning in the last several years. These include recent E. coli and Salmonella outbreaks leading to the recall of tremendous amounts of food throughout the US. Notably, Salmonella in peanut products and E. coli in ground beef both originated in US commercial food manufacturers as a result of poor hygiene and lack of mandatory safety regulations. Worse still, it took unconscionably long for the FDA to track down exactly where the problem started, leading to a much larger outbreak than necessary.
To prevent this from happening again, the new legislation calls for a Reportable Food Registry to be established and overseen by the FDA. This registry would ensure that any outbreak of food poisoning or adulterated food would be instantly reported to the FDA, which would then be able to use the registry to track down where the adulterated food came from, what other foods it might have come in contact with or been used in, and what distributors to alert. Not only would this increase the response time of the FDA, it would also allow traceability for the agency such that random testing of large numbers of those 150,000 individual commercial food manufacturers would not be required. If a tomato in Denver turned up positive for Salmonella, FDA scientists could quickly determine that it came from a wholesaler in Texas who purchased it from a grower in Louisiana. From there, all tomatoes that came from that grower or that passed through that wholesaler would be identified and the distributors notified to pull the tomatoes off their shelves.
This is a massive undertaking but a significant benefit to the food safety network in the US. Previously it might have taken FDA scientists weeks to trace a single infected tomato back to that grower in Louisiana, and in that time panicked distributors might destroy untold volumes of perfectly safe tomatoes, costing the food industry huge amounts of money. With the Registry, that process might take less than 48 hours, and the cost savings to distributors and wholesalers is the reason that the food industry generally supports this legislation.
One particular area of concern for the Obama administration is eggs – specifically, chickens, eggs, and Salmonella. It has been known for twenty years that infected chicks produce Salmonella-laden eggs that cannot be detected easily by the current food safety inspection systems in place. The new legislation mandates that egg growers take steps to eliminate rodents (a prime source of Salmonella contamination) and only purchase chicks from growers who also take steps to monitor Salmonella among their stock. Additional regulations require refrigeration during more of the lifespan of an egg, something that about half of all egg producers already do voluntarily and which would reduce the potential for Salmonella growth. As mentioned above, egg growers are generally in favor of these regulations – even though it will cost them some money for testing and prevention, they believe the increase in public confidence will more than make up for the estimated one-cent per dozen increase in the cost of eggs.
They’re almost certainly right. In this case, it doesn’t matter whether the chicken or the egg came first, so long as both of them come before the Salmonella.
For more information:
FDA Reportable Food Registry
Article from The Washington Post on the new legislation
New York Times article focusing on egg safety regulations
© A Quantum of Science / P. Smalley
Reproduction with attribution is appreciation
Sweeping and ambitious, administration regulations would enact mandatory oversight and tracking of critical foods
Today the Obama administration announced a major overhaul of the US food safety system. Overseen almost entirely by the FDA, some 150,000 individual commercial food producers would be subject to sweeping new regulations that would require traceability for all food and food additives sold in the US. This is a significant increase in the level of government oversight of the food industry and is a response to several high-profile outbreaks of food poisoning in the last several years. These include recent E. coli and Salmonella outbreaks leading to the recall of tremendous amounts of food throughout the US. Notably, Salmonella in peanut products and E. coli in ground beef both originated in US commercial food manufacturers as a result of poor hygiene and lack of mandatory safety regulations. Worse still, it took unconscionably long for the FDA to track down exactly where the problem started, leading to a much larger outbreak than necessary.
To prevent this from happening again, the new legislation calls for a Reportable Food Registry to be established and overseen by the FDA. This registry would ensure that any outbreak of food poisoning or adulterated food would be instantly reported to the FDA, which would then be able to use the registry to track down where the adulterated food came from, what other foods it might have come in contact with or been used in, and what distributors to alert. Not only would this increase the response time of the FDA, it would also allow traceability for the agency such that random testing of large numbers of those 150,000 individual commercial food manufacturers would not be required. If a tomato in Denver turned up positive for Salmonella, FDA scientists could quickly determine that it came from a wholesaler in Texas who purchased it from a grower in Louisiana. From there, all tomatoes that came from that grower or that passed through that wholesaler would be identified and the distributors notified to pull the tomatoes off their shelves.
This is a massive undertaking but a significant benefit to the food safety network in the US. Previously it might have taken FDA scientists weeks to trace a single infected tomato back to that grower in Louisiana, and in that time panicked distributors might destroy untold volumes of perfectly safe tomatoes, costing the food industry huge amounts of money. With the Registry, that process might take less than 48 hours, and the cost savings to distributors and wholesalers is the reason that the food industry generally supports this legislation.
One particular area of concern for the Obama administration is eggs – specifically, chickens, eggs, and Salmonella. It has been known for twenty years that infected chicks produce Salmonella-laden eggs that cannot be detected easily by the current food safety inspection systems in place. The new legislation mandates that egg growers take steps to eliminate rodents (a prime source of Salmonella contamination) and only purchase chicks from growers who also take steps to monitor Salmonella among their stock. Additional regulations require refrigeration during more of the lifespan of an egg, something that about half of all egg producers already do voluntarily and which would reduce the potential for Salmonella growth. As mentioned above, egg growers are generally in favor of these regulations – even though it will cost them some money for testing and prevention, they believe the increase in public confidence will more than make up for the estimated one-cent per dozen increase in the cost of eggs.
They’re almost certainly right. In this case, it doesn’t matter whether the chicken or the egg came first, so long as both of them come before the Salmonella.
For more information:
FDA Reportable Food Registry
Article from The Washington Post on the new legislation
New York Times article focusing on egg safety regulations
© A Quantum of Science / P. Smalley
Reproduction with attribution is appreciation
Monday, July 6, 2009
Newest Alzheimer's Drug: Coffee?
A QUANTUM OF SCIENCE
New research suggests caffeine may not only protect but can also reverse Alzheimer's Disease symptoms
Today's issue of the Journal of Alzheimer's Disease contains two reports involving the effects of caffeine on mice bred to mimic the biochemical degeneration of cognition found in human Alzheimer's disease. Briefly, the major source of this neural degeneration is the accumulation of a protein called Amyloid-β (or Aβ). A natural protein, Aβ can sometimes mis-fold and in that state becomes impervious to the normal cellular processes that break down aging proteins for recycling. Because it cannot be broken down, mis-folded Aβ accumulates and eventually causes cell death in the tissues surrounding it. Alzheimer's disease results when this takes place in brain tissue.
Researchers are interested in the process by which Aβ mis-folds, accumulates and - just possibly - might be eradicated. In the studies published today in the Journal of Alzheimer's Disease, researchers found that caffeine can not only protect Alzheimer's-prone mice from the accumulation of Aβ, but can even reduce Aβ levels in the brains and blood of mice who already have advanced Alzheimer's conditions. This is not the first report of caffeine's effects, but the two studies are back-to-back illustrations of the growing body of evidence linking caffeine to treatment for Alzheimer's even after the condition is diagnosed. Additionally, the levels of caffeine used in this study are relevant - the equivalent of about five cups of coffee per day for a human. This is exciting as it suggests that caffeine treatment might be possible without resorting to levels so high as to cause dangerous side-effects to humans.
For more information:
Caffeine Reverses Cognitive Impairment and Decreases Brain Amyloid-β Levels in Aged Alzheimer’s Disease Mice (Arendash et al)
Caffeine Suppresses Amyloid-β Levels in Plasma and Brain of Alzheimer’s Disease Transgenic Mice (Chuanhai et al)
© A Quantum of Science / P. Smalley
Reproduction with attribution is appreciation!
New research suggests caffeine may not only protect but can also reverse Alzheimer's Disease symptoms
Today's issue of the Journal of Alzheimer's Disease contains two reports involving the effects of caffeine on mice bred to mimic the biochemical degeneration of cognition found in human Alzheimer's disease. Briefly, the major source of this neural degeneration is the accumulation of a protein called Amyloid-β (or Aβ). A natural protein, Aβ can sometimes mis-fold and in that state becomes impervious to the normal cellular processes that break down aging proteins for recycling. Because it cannot be broken down, mis-folded Aβ accumulates and eventually causes cell death in the tissues surrounding it. Alzheimer's disease results when this takes place in brain tissue.
Researchers are interested in the process by which Aβ mis-folds, accumulates and - just possibly - might be eradicated. In the studies published today in the Journal of Alzheimer's Disease, researchers found that caffeine can not only protect Alzheimer's-prone mice from the accumulation of Aβ, but can even reduce Aβ levels in the brains and blood of mice who already have advanced Alzheimer's conditions. This is not the first report of caffeine's effects, but the two studies are back-to-back illustrations of the growing body of evidence linking caffeine to treatment for Alzheimer's even after the condition is diagnosed. Additionally, the levels of caffeine used in this study are relevant - the equivalent of about five cups of coffee per day for a human. This is exciting as it suggests that caffeine treatment might be possible without resorting to levels so high as to cause dangerous side-effects to humans.
For more information:
Caffeine Reverses Cognitive Impairment and Decreases Brain Amyloid-β Levels in Aged Alzheimer’s Disease Mice (Arendash et al)
Caffeine Suppresses Amyloid-β Levels in Plasma and Brain of Alzheimer’s Disease Transgenic Mice (Chuanhai et al)
© A Quantum of Science / P. Smalley
Reproduction with attribution is appreciation!
Thursday, July 2, 2009
Music Gene
A Genetic Basis for Music?
A QUANTUM OF SCIENCE
Musical legacy found in a gene associated with social interaction traits – including love
Researchers in Finland recently reported a study in which 19 Finnish familes (343 individuals) with many professional or active amateur musicians among them were studied for genetic similarities. The study found that a single gene, AVPR1A (for arginine vasopressin receptor 1A), held a strong statistical correlation to creative musical abilities such as pitch, tempo and composition, especially when members of multiple generations all shared musical ability. So what is arginine vasopressin?
Peptide hormones, of which the vasopressins are a subfamily, are composed of short cyclic chains of amino acids (nine, in this case) and regulate a number of physiological functions. Arginine vasopression (abbreviated AVP) controls hydration through kidney function, including the stimulation of urine dilution and concentration in balance with the body’s need for extra water. For this activity it is secreted into the bloodstream, but some AVP is also found in the brain, where it binds to a specialized receptor – the one encoded by the gene AVPR1A. Binding of AVP to AVPR1A stimulates the brain to release neurotransmitters that play into "social behavior" responses, including the mate bonding behavior found in voles and, to a greater or lesser extent, in humans. Some studies have even suggested that these same neurotransmitters play a role in feelings of altruism, or love.
Is there a single gene that determines who is musical and who is not? These findings are preliminary and far from exhaustive, but they point to a biological function encouraging the spread and preservation of the AVPR1A gene. If, as suggested, the AVP/AVPR1A peptide hormone receptor plays a role in social behavior and other emotional attachment activities in higher mammals, it could easily be linked to the development of early human societies via the universal language: music.
For more information:
Original PLOS article
© A Quantum of Science / P. Smalley
Reproduction with attribution is appreciation
A QUANTUM OF SCIENCE
Musical legacy found in a gene associated with social interaction traits – including love
Researchers in Finland recently reported a study in which 19 Finnish familes (343 individuals) with many professional or active amateur musicians among them were studied for genetic similarities. The study found that a single gene, AVPR1A (for arginine vasopressin receptor 1A), held a strong statistical correlation to creative musical abilities such as pitch, tempo and composition, especially when members of multiple generations all shared musical ability. So what is arginine vasopressin?
Peptide hormones, of which the vasopressins are a subfamily, are composed of short cyclic chains of amino acids (nine, in this case) and regulate a number of physiological functions. Arginine vasopression (abbreviated AVP) controls hydration through kidney function, including the stimulation of urine dilution and concentration in balance with the body’s need for extra water. For this activity it is secreted into the bloodstream, but some AVP is also found in the brain, where it binds to a specialized receptor – the one encoded by the gene AVPR1A. Binding of AVP to AVPR1A stimulates the brain to release neurotransmitters that play into "social behavior" responses, including the mate bonding behavior found in voles and, to a greater or lesser extent, in humans. Some studies have even suggested that these same neurotransmitters play a role in feelings of altruism, or love.
Is there a single gene that determines who is musical and who is not? These findings are preliminary and far from exhaustive, but they point to a biological function encouraging the spread and preservation of the AVPR1A gene. If, as suggested, the AVP/AVPR1A peptide hormone receptor plays a role in social behavior and other emotional attachment activities in higher mammals, it could easily be linked to the development of early human societies via the universal language: music.
For more information:
Original PLOS article
© A Quantum of Science / P. Smalley
Reproduction with attribution is appreciation
Tuesday, June 30, 2009
Newest AIDS drug: Sugar?
A QUANTUM OF SCIENCE
Common polysaccharide prevents HIV infection in mice
Researchers at Meharry Medical College School of Medicine in Nashville recently reported that HIV-1 infections were blocked in mice by a surprising compound: cyclodextrin, a common cyclic sugar used extensively in food, pharmaceuticals and commercial products such as dryer sheets and Febreze.
The structure of cyclodextrin is a hollow ring, perfect for complexing hydrophobic molecules (such as fragrances, in the case of Febreze) and binding them tightly. This also makes cyclodextrin a good carrier molecule for pharmaceuticals, encapsulating drugs and aiding their delivery to different parts of the body. Surprisingly, the use of cyclodextrin in the food industry held the key to its role in preventing HIV infection. In the food industry cyclodextrins are employed for the preparation of cholesterol free products, allowing cholesterol to be sequestered inside the hollow ring of cyclodextrin and more easily removed from the food matrix.
Researchers have known for some time that there was a link between cholesterol and HIV infection. Cholesterol is an essential part of cell membranes, helping them stay fluid and permeable for normal trans-membrane traffic. Lipid rafts, a specialized structure rich in cholesterol, is required for HIV-1 to infect new cells. Though the research is still preliminary, cyclodextrin’s ability to bind and sequester cholesterol appears to play a role in preventing successful HIV infections. Trials in mice demonstrated a transient, reversible protective effect when female mice were challenged with HIV-laden semen. Similar experiments in primates have not fared as well, but issues with those studies have sparked several more extensive trials and the scientific community is abuzz with the possibilities.
Among the most exciting properties of cyclodextrin from a pharmaceutical standpoint is its safety. Discovered in 1891, cyclodextrins have been used for decades in foods and medicines. Its toxicity is extremely low, even when used in high dosages, and since it is composed entirely of sugar molecules there is little chance of complications or immune reactions. Only time will tell whether this humble molecule will find a new role in the prevention of HIV infections, but pharmaceutical giant Johnson & Johnson is already pursuing it as a therapeutic and prophylactic.
For more information:
http://www.the-scientist.com/templates/trackable/display/blog.jsp?type=blog&o_url=blog/display/55807&id=55807
© A Quantum of Science / P. Smalley (2009)
Reproduction with attribution is appreciation!
Common polysaccharide prevents HIV infection in mice
Researchers at Meharry Medical College School of Medicine in Nashville recently reported that HIV-1 infections were blocked in mice by a surprising compound: cyclodextrin, a common cyclic sugar used extensively in food, pharmaceuticals and commercial products such as dryer sheets and Febreze.
The structure of cyclodextrin is a hollow ring, perfect for complexing hydrophobic molecules (such as fragrances, in the case of Febreze) and binding them tightly. This also makes cyclodextrin a good carrier molecule for pharmaceuticals, encapsulating drugs and aiding their delivery to different parts of the body. Surprisingly, the use of cyclodextrin in the food industry held the key to its role in preventing HIV infection. In the food industry cyclodextrins are employed for the preparation of cholesterol free products, allowing cholesterol to be sequestered inside the hollow ring of cyclodextrin and more easily removed from the food matrix.
Researchers have known for some time that there was a link between cholesterol and HIV infection. Cholesterol is an essential part of cell membranes, helping them stay fluid and permeable for normal trans-membrane traffic. Lipid rafts, a specialized structure rich in cholesterol, is required for HIV-1 to infect new cells. Though the research is still preliminary, cyclodextrin’s ability to bind and sequester cholesterol appears to play a role in preventing successful HIV infections. Trials in mice demonstrated a transient, reversible protective effect when female mice were challenged with HIV-laden semen. Similar experiments in primates have not fared as well, but issues with those studies have sparked several more extensive trials and the scientific community is abuzz with the possibilities.
Among the most exciting properties of cyclodextrin from a pharmaceutical standpoint is its safety. Discovered in 1891, cyclodextrins have been used for decades in foods and medicines. Its toxicity is extremely low, even when used in high dosages, and since it is composed entirely of sugar molecules there is little chance of complications or immune reactions. Only time will tell whether this humble molecule will find a new role in the prevention of HIV infections, but pharmaceutical giant Johnson & Johnson is already pursuing it as a therapeutic and prophylactic.
For more information:
http://www.the-scientist.com/templates/trackable/display/blog.jsp?type=blog&o_url=blog/display/55807&id=55807
© A Quantum of Science / P. Smalley (2009)
Reproduction with attribution is appreciation!
Thursday, May 28, 2009
Quantum: Ancient immunity
A QUANTUM OF SCIENCE
New findings show adaptive immune system may not be new invention
Recently, scientists at Emory University in Atlanta reported that lampreys - a cartilaginous fish which evolved around 500 million years ago - is the oldest organism yet found to possess an adaptive immune system like that of humans. Previously, the adaptive immune system was believed to have originated in sharks, which evolved around 400 million years ago. This extra 100 million years is a big deal because the lamprey is a much earlier splinter from the vertebrate branch of the tree of life, and could mean that other even more ancient predecessors had already figured out how to "record" microbial invaders and repel them better in future infections.
Another interesting note: the age of cartilaginous fishes was known as the Silurian period, a time culminating in the so-called Law Event in which approximately 60% of aquatic species became extinct through a series of rapid climatic changes. Could the adaptive immune system have helped lampreys and sharks survive?
For more information:
The Scientist: Ancient organism, modern immunity
© A Quantum of Science / Peter Smalley (2009)
Reproduction with attribution is appreciation
New findings show adaptive immune system may not be new invention
Recently, scientists at Emory University in Atlanta reported that lampreys - a cartilaginous fish which evolved around 500 million years ago - is the oldest organism yet found to possess an adaptive immune system like that of humans. Previously, the adaptive immune system was believed to have originated in sharks, which evolved around 400 million years ago. This extra 100 million years is a big deal because the lamprey is a much earlier splinter from the vertebrate branch of the tree of life, and could mean that other even more ancient predecessors had already figured out how to "record" microbial invaders and repel them better in future infections.
Another interesting note: the age of cartilaginous fishes was known as the Silurian period, a time culminating in the so-called Law Event in which approximately 60% of aquatic species became extinct through a series of rapid climatic changes. Could the adaptive immune system have helped lampreys and sharks survive?
For more information:
The Scientist: Ancient organism, modern immunity
© A Quantum of Science / Peter Smalley (2009)
Reproduction with attribution is appreciation
Tuesday, May 26, 2009
Curing the Mosquito
A QUANTUM OF SCIENCE
How can bacteria help protect humans from malaria?
Malaria is a deadly but neglected tropical disease that has received more money and attention in the last decade than in perhaps the preceding century. The disease is spread by mosquitoes in whose gut live one or more of five protozoan species of the Plasmodium genus. As a protozoa, it is neither a virus nor a bacteria but more like an amoeba or an algae, and thus it is more difficult to fight because its cells look more like human ones than either viruses or bacteria. Malaria is contracted by 350-500 million people every year, and approximately 1-3 million die of it annually - mostly sub-Saharan children. Now a scientist at the Johns Hopkins University Malaria Research Institute think he might have a unique way to help break the cycle of malarial infection.
The answer? Cure the mosquito.
For a long time it was thought that malaria could be controlled by using insecticides and bed screens to keep the mosquitoes away, but these approaches have both proven only partially effective. Insecticides also have their own toll on both human health and the environment, and rapidly become ineffective. But Dr. George Dimopoulos has found a species of bacteria living in the gut of the mosquito whose presence seems to inhibit the growth of the malaria protozoa. When he treated mosquitoes with an antibiotic, the bacteria died and the protozoa multiplied manyfold, making the mosquito a much deadlier vector for the disease. By helping this specific bacterium to stimulate the mosquito's immune system and cure it of the protozoans it carries, Dr. Dimopoulos believes, the spread of malaria could be controlled more effectively than with insecticides or bed screens alone.
If so, this could be a new and unprecedented breakthrough in fighting malaria, one of the great scourges of Africa.
For more information:
VOA News article
Public Library of Science article by Dr. Dimopoulos
Wikipedia entry on protozoa
© A Quantum of Science / Peter Smalley (2009)
Reproduction with attribution is appreciation
How can bacteria help protect humans from malaria?
Malaria is a deadly but neglected tropical disease that has received more money and attention in the last decade than in perhaps the preceding century. The disease is spread by mosquitoes in whose gut live one or more of five protozoan species of the Plasmodium genus. As a protozoa, it is neither a virus nor a bacteria but more like an amoeba or an algae, and thus it is more difficult to fight because its cells look more like human ones than either viruses or bacteria. Malaria is contracted by 350-500 million people every year, and approximately 1-3 million die of it annually - mostly sub-Saharan children. Now a scientist at the Johns Hopkins University Malaria Research Institute think he might have a unique way to help break the cycle of malarial infection.
The answer? Cure the mosquito.
For a long time it was thought that malaria could be controlled by using insecticides and bed screens to keep the mosquitoes away, but these approaches have both proven only partially effective. Insecticides also have their own toll on both human health and the environment, and rapidly become ineffective. But Dr. George Dimopoulos has found a species of bacteria living in the gut of the mosquito whose presence seems to inhibit the growth of the malaria protozoa. When he treated mosquitoes with an antibiotic, the bacteria died and the protozoa multiplied manyfold, making the mosquito a much deadlier vector for the disease. By helping this specific bacterium to stimulate the mosquito's immune system and cure it of the protozoans it carries, Dr. Dimopoulos believes, the spread of malaria could be controlled more effectively than with insecticides or bed screens alone.
If so, this could be a new and unprecedented breakthrough in fighting malaria, one of the great scourges of Africa.
For more information:
VOA News article
Public Library of Science article by Dr. Dimopoulos
Wikipedia entry on protozoa
© A Quantum of Science / Peter Smalley (2009)
Reproduction with attribution is appreciation
Sunday, May 24, 2009
A Cure for the Common Cancer
A QUANTUM OF SCIENCE
What can the common cold do to help fight cancer?
Behold one of the most successful organisms in the history of the world: the humble adenovirus, better known as the cold. Human have recorded suffering from this virus since at least Hippocritas, and likely much earlier. Every year humans around the world come down with runny noses, coughs and fevers associated with the cold. And then they spread it to others, and recover - until the next round. Adenoviruses are among the handful of true success stories in biology. Now, scientists have found a way to harness the infectivity of the common cold to make it serve a therapeutic function, not an epidemiological one.
Recently, a group of scientists led by Dr. Leonard Seymour of Oxford University reported successfully removing the "disease" genes from a adenovirus and replacing them with genes for cancerous proteins. Why would this help? In the same way that your body's immune system eventually learns to recognize and attack normal adenoviruses that manage to infect you, the modified adenovirus contains cancer-linked genes that provide the immune system with the opportunity to "learn" that these proteins are invaders to be fought, potentially turning the immune system into the most potent and selective anti-cancer fighter possible.
Scientists have managed similar feats before but to do so they have had to weaken the virus, making it less effective at stimulating the immune system and teaching it to recognize cancer proteins as invaders to be fought. With this achievement, Dr. Seymour and his collaborators have taken a large step forward into a burgeoning field of therapeutics drawn from biological strategies older than humanity itself.
For more inforation:
http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1000440
(C) AQOS / Peter Smalley (2009)
What can the common cold do to help fight cancer?
Behold one of the most successful organisms in the history of the world: the humble adenovirus, better known as the cold. Human have recorded suffering from this virus since at least Hippocritas, and likely much earlier. Every year humans around the world come down with runny noses, coughs and fevers associated with the cold. And then they spread it to others, and recover - until the next round. Adenoviruses are among the handful of true success stories in biology. Now, scientists have found a way to harness the infectivity of the common cold to make it serve a therapeutic function, not an epidemiological one.
Recently, a group of scientists led by Dr. Leonard Seymour of Oxford University reported successfully removing the "disease" genes from a adenovirus and replacing them with genes for cancerous proteins. Why would this help? In the same way that your body's immune system eventually learns to recognize and attack normal adenoviruses that manage to infect you, the modified adenovirus contains cancer-linked genes that provide the immune system with the opportunity to "learn" that these proteins are invaders to be fought, potentially turning the immune system into the most potent and selective anti-cancer fighter possible.
Scientists have managed similar feats before but to do so they have had to weaken the virus, making it less effective at stimulating the immune system and teaching it to recognize cancer proteins as invaders to be fought. With this achievement, Dr. Seymour and his collaborators have taken a large step forward into a burgeoning field of therapeutics drawn from biological strategies older than humanity itself.
For more inforation:
http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1000440
(C) AQOS / Peter Smalley (2009)
Thursday, May 21, 2009
A single amino acid
A QUANTUM OF SCIENCE
Why does the more lethal H5N1 Avian flu not infect humans more readily?
Several references have been made now to the "nightmare scenario" in which genes from the more lethal Avian flu (H5N1) reassort with the less dangerous but more infective Swine flu (H1N1), generating a hybrid that is both lethal and infective. We have yet to talk much about why the H5N1 strain is harder for people to catch – so hard that in some years there are only a single-digit number of cases.
Certainly, the lethality of H5N1 inhibits its spread. In epidemiological terms, the virus kills faster than it spreads, leading to a reproduction number at or below one. In a recent paper, researchers show that a single amino acid change in the sequence of the viral polymerase gene (PB2) results in a dramatic difference in both temperature tolerance and infectivity.
Scientists at University of North Carolina at Chapel Hill found that the H5N1 virus required the higher temperatures found in its bird hosts (around 40 degrees Celsius) in order to be highly infective. At 32 degrees Celsius - the temperature of the cells found in human nasal passages called HAE, or human airway epithelium – the H5N1 virus became sticky and did not effectively infect those cells. The reason for this? A single amino acid at position 627 of the polymerase protein of the H5N1 virus was changed, allowing it to be glycosylated - chemically modified to bear a particular sugar residue. Researchers were able to prove this by genetically altering a human influenza virus (which infected cells optimally at 32 degrees Celsius) at position 627, changing just that one amino acid to one that could be glycosylated. The resulting human virus was not capable of creating an infection in human airway epithelial cells, demonstrating an attenuation of the formerly infective human influenza virus. Further modification of viral coat proteins fully attained an "avian" level of temperature sensitivity.
This research is important because it significantly adds to our understanding of the molecular process by which the influenza virus mounts a successful infection in either of its principal hosts (birds or humans). Scientists who sequence previously unknown strains of influenza isolated from patients can now rapidly assess the polymerase gene (PB2) and determine quickly whether it is an avian strain or one more evolved for humans. Not only the treatments recommended but also the course of a widespread epidemiological event could be affected by this. Further, scientists searching for the molecular keys to understanding the mutations of various influenza strains can now look more effectively for such alterations, granting insight into the process of interspecies spread of the virus.
Perhaps most importantly, these findings help to partially allay fears that H5N1 is likely to reassort with H1N1 – since avian flu infects HAE cells poorly due to their intolerance for colder temperatures, we are less likely to endure that kind of hybrid virus.
For more information:
Avian Influenza Virus Glycoproteins Restrict Virus Replication and Spread through Human Airway Epithelium at Temperatures of the Proximal Airways.
© A Quantum of Science / Peter Smalley (2009)
Reproduction with attribution is appreciation
Why does the more lethal H5N1 Avian flu not infect humans more readily?
Several references have been made now to the "nightmare scenario" in which genes from the more lethal Avian flu (H5N1) reassort with the less dangerous but more infective Swine flu (H1N1), generating a hybrid that is both lethal and infective. We have yet to talk much about why the H5N1 strain is harder for people to catch – so hard that in some years there are only a single-digit number of cases.
Certainly, the lethality of H5N1 inhibits its spread. In epidemiological terms, the virus kills faster than it spreads, leading to a reproduction number at or below one. In a recent paper, researchers show that a single amino acid change in the sequence of the viral polymerase gene (PB2) results in a dramatic difference in both temperature tolerance and infectivity.
Scientists at University of North Carolina at Chapel Hill found that the H5N1 virus required the higher temperatures found in its bird hosts (around 40 degrees Celsius) in order to be highly infective. At 32 degrees Celsius - the temperature of the cells found in human nasal passages called HAE, or human airway epithelium – the H5N1 virus became sticky and did not effectively infect those cells. The reason for this? A single amino acid at position 627 of the polymerase protein of the H5N1 virus was changed, allowing it to be glycosylated - chemically modified to bear a particular sugar residue. Researchers were able to prove this by genetically altering a human influenza virus (which infected cells optimally at 32 degrees Celsius) at position 627, changing just that one amino acid to one that could be glycosylated. The resulting human virus was not capable of creating an infection in human airway epithelial cells, demonstrating an attenuation of the formerly infective human influenza virus. Further modification of viral coat proteins fully attained an "avian" level of temperature sensitivity.
This research is important because it significantly adds to our understanding of the molecular process by which the influenza virus mounts a successful infection in either of its principal hosts (birds or humans). Scientists who sequence previously unknown strains of influenza isolated from patients can now rapidly assess the polymerase gene (PB2) and determine quickly whether it is an avian strain or one more evolved for humans. Not only the treatments recommended but also the course of a widespread epidemiological event could be affected by this. Further, scientists searching for the molecular keys to understanding the mutations of various influenza strains can now look more effectively for such alterations, granting insight into the process of interspecies spread of the virus.
Perhaps most importantly, these findings help to partially allay fears that H5N1 is likely to reassort with H1N1 – since avian flu infects HAE cells poorly due to their intolerance for colder temperatures, we are less likely to endure that kind of hybrid virus.
For more information:
Avian Influenza Virus Glycoproteins Restrict Virus Replication and Spread through Human Airway Epithelium at Temperatures of the Proximal Airways.
© A Quantum of Science / Peter Smalley (2009)
Reproduction with attribution is appreciation
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