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!
Tuesday, June 30, 2009
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
Wednesday, May 20, 2009
Mapping H1N1
A QUANTUM OF SCIENCE
Where in the world is H1N1?
The spread of H1N1 around the world has significant implications for the etiology and epidemiology of the disease, as well as the global health infrastructure’s response to it. Raw numbers alone do not tell the story as well as this single image, taken from the WHO pandemic alert and response website.
This map is current: as of today there are a global total of 10,243 laboratory-confirmed cases of H1N1 influenza that have been reported to the WHO, including 80 deaths (making the global mortality rate one death out of every 128 cases). While the actual number of total cases is inevitably somewhat higher due to the lagging nature of lab confirmations and reporting, what is more interesting is the distribution of the cases – and deaths – and what this might tell us about the past and future of H1N1.
Originally dubbed as Swine Flu, the official name for this strain of H1N1 is North American influenza, and indeed the overwhelming majority of the cases are in North America (93.8%). What is interesting to note is that 79 of the 80 confirmed deaths are also in North America (98.75%). Digging a little deeper into the distribution of deaths, we find that this is due to the large contribution of deaths from H1N1 in Mexico, where the mortality rate is one death for every 50.6 cases. That is two and a half times the global mortality rate, and eighteen times the mortality rate in the adjacent United States. With the sequencing of the H1N1 genome in Canada that was announced yesterday, no significant differences were found in strains isolated in Mexico versus those in the United States or Canada. While this is somewhat reassuring because it means there is not a more virulent strain on the loose in Mexico, it requires a different explanation. Some authorities have suggested Mexico has deficiencies in its health infrastructure, but others cite a cultural inhibition that may play a more pervasive role in preventing infected persons from seeking help until it is too late. In either case, however, countries with similar health infrastructures and cultures would be expected to have a similar mortality rate, and this has not yet been borne out (as the map’s number for Central and South America show).
Another point of interest brought out by the map of H1N1 cases to date are the non-North American hot spots. Japan is the leader of these, with 210 cases, followed almost evenly by Spain (107) and the United Kingdom (102). What is interesting about this is the far-flung locations of the hotspots outside North America. Nothing like the close distribution of cases in Mexico-US-Canada have been seen in these Asian and European hotspots. This could mean that there is something particular to North America that supports the infectivity of the viral strain; or it could mean that it is simply too soon, and the neighbors of these hotspots will soon show a commensurate rise in cases. It is worth noting that strains of influenza are known to show a strong geographical preference; the deadly Bird flu (H5N1) is almost unknown outside of the Far East, for reasons that scientists are still trying to elucidate. This also brings up the potential for reassortment of viral genes between H1N1 and H5N1, now that the former has entered the latter’s territory. Still, Japan has been aggressive about treating flu cases and currently Roche (the maker of Tamiflu) estimates that 35 million of the 50 million people who have been treated with Tamiflu are in Japan. It can be hoped that this aggressive treatment schedule will be effective in containing the possible hybridization of H1N1 with H5N1.
For more information:
WHO Epidemic and Pandemic Alert and Response
WHO H1N1 map (20-May-2009 version)
Tamiflu (Oseltamivir) information, including use in Japan
© A Quantum of Science / Peter Smalley (2009)
Reproduction with attribution is appreciation
Where in the world is H1N1?
The spread of H1N1 around the world has significant implications for the etiology and epidemiology of the disease, as well as the global health infrastructure’s response to it. Raw numbers alone do not tell the story as well as this single image, taken from the WHO pandemic alert and response website.
This map is current: as of today there are a global total of 10,243 laboratory-confirmed cases of H1N1 influenza that have been reported to the WHO, including 80 deaths (making the global mortality rate one death out of every 128 cases). While the actual number of total cases is inevitably somewhat higher due to the lagging nature of lab confirmations and reporting, what is more interesting is the distribution of the cases – and deaths – and what this might tell us about the past and future of H1N1.
Originally dubbed as Swine Flu, the official name for this strain of H1N1 is North American influenza, and indeed the overwhelming majority of the cases are in North America (93.8%). What is interesting to note is that 79 of the 80 confirmed deaths are also in North America (98.75%). Digging a little deeper into the distribution of deaths, we find that this is due to the large contribution of deaths from H1N1 in Mexico, where the mortality rate is one death for every 50.6 cases. That is two and a half times the global mortality rate, and eighteen times the mortality rate in the adjacent United States. With the sequencing of the H1N1 genome in Canada that was announced yesterday, no significant differences were found in strains isolated in Mexico versus those in the United States or Canada. While this is somewhat reassuring because it means there is not a more virulent strain on the loose in Mexico, it requires a different explanation. Some authorities have suggested Mexico has deficiencies in its health infrastructure, but others cite a cultural inhibition that may play a more pervasive role in preventing infected persons from seeking help until it is too late. In either case, however, countries with similar health infrastructures and cultures would be expected to have a similar mortality rate, and this has not yet been borne out (as the map’s number for Central and South America show).
Another point of interest brought out by the map of H1N1 cases to date are the non-North American hot spots. Japan is the leader of these, with 210 cases, followed almost evenly by Spain (107) and the United Kingdom (102). What is interesting about this is the far-flung locations of the hotspots outside North America. Nothing like the close distribution of cases in Mexico-US-Canada have been seen in these Asian and European hotspots. This could mean that there is something particular to North America that supports the infectivity of the viral strain; or it could mean that it is simply too soon, and the neighbors of these hotspots will soon show a commensurate rise in cases. It is worth noting that strains of influenza are known to show a strong geographical preference; the deadly Bird flu (H5N1) is almost unknown outside of the Far East, for reasons that scientists are still trying to elucidate. This also brings up the potential for reassortment of viral genes between H1N1 and H5N1, now that the former has entered the latter’s territory. Still, Japan has been aggressive about treating flu cases and currently Roche (the maker of Tamiflu) estimates that 35 million of the 50 million people who have been treated with Tamiflu are in Japan. It can be hoped that this aggressive treatment schedule will be effective in containing the possible hybridization of H1N1 with H5N1.
For more information:
WHO Epidemic and Pandemic Alert and Response
WHO H1N1 map (20-May-2009 version)
Tamiflu (Oseltamivir) information, including use in Japan
© A Quantum of Science / Peter Smalley (2009)
Reproduction with attribution is appreciation
Tuesday, May 19, 2009
Canadian scientists sequence H1N1 genome
A QUANTUM OF SCIENCE
Now we know the complete blueprint for H1N1; now what?
Today it was announced that scientists in Canada have fully sequenced the entire genome of the H1N1 influenza virus. While it's not the first viral genome to be fully sequenced, it is a landmark achievement and all the more so for having been completed in one week of around-the-clock work by scientists at Canada's National Microbiology Laboratory in Winnipeg. This is, as the saying goes, kind of a big deal.
These findings shed some intriguing light on the outbreak of H1N1 but raises even more questions, as most scientific discoveries do. For example, researchers found virtually no difference between the Mexican strains and those occurring in the US or Canada. Why, then, have so many more cases in Mexico proven fatal? The answers may not lie in the genes themselves, but rather in differences of health infrastructure and health policy. Benefits of this breakthrough include faster analysis of future strains, a better understanding of how and why H1N1 mutations or reassortments occur, and a better H1N1 vaccine - with this last being of crucial importance as major pharmaceutical companies begin the laborious process of choosing which sequences to use for their vaccines. With an improved understanding of the variations in the H1N1 genome, conserved sequences can be selected for use vaccines, resulting in a stronger, more robust protection against future infection.
Perhaps it is a little cynical, but one might consider that the timing of this announcement seems a little too convenient considering that today is the second day of the 62nd World Health Assembly, the annual meeting of the World Health Organization whose handling of the H1N1 outbreak has been criticized by many science and health professionals. Then again, maybe it is simply a case of serendipity; regardless, it is good news and that's worth remembering.
Plus, if you want to apply for the position of Viral Genome Curator at a company in Bethesda, MD, you now have one more fully-sequenced genome to add to the list.
For more information:
http://www.canada.com/Health/Canadian+completes+sequencing+virus/1569084/story.html
© A Quantum of Science / Peter Smalley (2009)
Reproduction with attribution is appreciation
Now we know the complete blueprint for H1N1; now what?
Today it was announced that scientists in Canada have fully sequenced the entire genome of the H1N1 influenza virus. While it's not the first viral genome to be fully sequenced, it is a landmark achievement and all the more so for having been completed in one week of around-the-clock work by scientists at Canada's National Microbiology Laboratory in Winnipeg. This is, as the saying goes, kind of a big deal.
These findings shed some intriguing light on the outbreak of H1N1 but raises even more questions, as most scientific discoveries do. For example, researchers found virtually no difference between the Mexican strains and those occurring in the US or Canada. Why, then, have so many more cases in Mexico proven fatal? The answers may not lie in the genes themselves, but rather in differences of health infrastructure and health policy. Benefits of this breakthrough include faster analysis of future strains, a better understanding of how and why H1N1 mutations or reassortments occur, and a better H1N1 vaccine - with this last being of crucial importance as major pharmaceutical companies begin the laborious process of choosing which sequences to use for their vaccines. With an improved understanding of the variations in the H1N1 genome, conserved sequences can be selected for use vaccines, resulting in a stronger, more robust protection against future infection.
Perhaps it is a little cynical, but one might consider that the timing of this announcement seems a little too convenient considering that today is the second day of the 62nd World Health Assembly, the annual meeting of the World Health Organization whose handling of the H1N1 outbreak has been criticized by many science and health professionals. Then again, maybe it is simply a case of serendipity; regardless, it is good news and that's worth remembering.
Plus, if you want to apply for the position of Viral Genome Curator at a company in Bethesda, MD, you now have one more fully-sequenced genome to add to the list.
For more information:
http://www.canada.com/Health/Canadian+completes+sequencing+virus/1569084/story.html
© A Quantum of Science / Peter Smalley (2009)
Reproduction with attribution is appreciation
Quantum: Influenza tutorial (powerpoint)
A QUANTUM OF SCIENCE
This powerpoint presentation may be a little advanced in places but there is some great information to be extracted even with just a casual viewing, especially among the pictures. The author, Dr. Mustafa Ababneh, is a molecular virologist at the Department of Veterinary Clinical Sciences, Jordan University of Science and Technology.
For more information:
Dr. Ababneh's publication record on PubMed
© A Quantum of Science / Peter Smalley (2009)
Reproduction with attribution is appreciation
This powerpoint presentation may be a little advanced in places but there is some great information to be extracted even with just a casual viewing, especially among the pictures. The author, Dr. Mustafa Ababneh, is a molecular virologist at the Department of Veterinary Clinical Sciences, Jordan University of Science and Technology.
For more information:
Dr. Ababneh's publication record on PubMed
© A Quantum of Science / Peter Smalley (2009)
Reproduction with attribution is appreciation
Quantum: flu expert fears H5N1 nightmare
A QUANTUM OF SCIENCE
What happens when the lethal but less-infective H5N1 strain of influenza mingles with the relatively benign but more-infective H1N1?
Dr. Yi Guan of Hong Kong Kong University is one of the leading flu experts in the world. His claim to fame was the isolation of the SARS virus in wild civets in 2003; his recommendation to eliminate the population of captive civets may have prevented a re-emergence of SARS since then. Now he has some strong criticisms of the World Health Organization's handling of H1N1, and worries about the potential for a sharing of lethal H5N1 genes with H1N1, which has proven itself far better at spreading itself around than H5N1.
The difference between the two strains' ability to infect may be in the gene encoding hemagglutinin, the protein that helps the virus get into cells and infect them. Recently published data shows that the genetic sequence for the hemagglutinin (HA) gene is only 9.7% similar between H5N1 and H1N1, by far the largest difference between their genetic codes. Because influenza is capable of rapid reassortment - the shuffling of genes like decks of cards - it may only be a matter of time before the HA gene from H1N1 is adopted by H5N1. That could have profoundly dire effects if experts like Dr. Guan are to be believed. So far the only ray of hope that nightmare scenario will not happen is the H1N1 seems restricted to North America, while H5N1 is only found in Asia. Critics of the WHO like Dr. Guan seem to be quite justified in calling for increased attention to transcontinental spread of H1N1 and more aggressive use of TamiFlu and other treatments to curb the spread of H1N1 into Asia.
More information:
http://blogs.sciencemag.org/scienceinsider/2009/05/exclusive-meet.html
© A Quantum of Science / Peter Smalley (2009)
Reproduction with attribution is appreciation
What happens when the lethal but less-infective H5N1 strain of influenza mingles with the relatively benign but more-infective H1N1?
Dr. Yi Guan of Hong Kong Kong University is one of the leading flu experts in the world. His claim to fame was the isolation of the SARS virus in wild civets in 2003; his recommendation to eliminate the population of captive civets may have prevented a re-emergence of SARS since then. Now he has some strong criticisms of the World Health Organization's handling of H1N1, and worries about the potential for a sharing of lethal H5N1 genes with H1N1, which has proven itself far better at spreading itself around than H5N1.
The difference between the two strains' ability to infect may be in the gene encoding hemagglutinin, the protein that helps the virus get into cells and infect them. Recently published data shows that the genetic sequence for the hemagglutinin (HA) gene is only 9.7% similar between H5N1 and H1N1, by far the largest difference between their genetic codes. Because influenza is capable of rapid reassortment - the shuffling of genes like decks of cards - it may only be a matter of time before the HA gene from H1N1 is adopted by H5N1. That could have profoundly dire effects if experts like Dr. Guan are to be believed. So far the only ray of hope that nightmare scenario will not happen is the H1N1 seems restricted to North America, while H5N1 is only found in Asia. Critics of the WHO like Dr. Guan seem to be quite justified in calling for increased attention to transcontinental spread of H1N1 and more aggressive use of TamiFlu and other treatments to curb the spread of H1N1 into Asia.
More information:
http://blogs.sciencemag.org/scienceinsider/2009/05/exclusive-meet.html
© A Quantum of Science / Peter Smalley (2009)
Reproduction with attribution is appreciation
Monday, May 18, 2009
Quantum: Counting H1N1
A QUANTUM OF SCIENCE
First let's tackle the jargon.
Prevalence is the total number of cases of a disease or infection in a given population. The important thing to remember about prevalence is that it is all the cases, not just the new ones, so the longer it takes to recover from a particular infection, the higher the prevalence will be. Most of the H1N1 figures you hear or read about are prevalence numbers, and as such are not as accurate a reflection as they might be.
Incidence is the rate at which new cases occur in a population, and is a better measure of how fast a disease is spreading because it takes out the duration-of-illness factor included in prevalence. Incidence is usually reported per capita ("3 new infections per 1000 people") or even with a time-element ("14 per 1000 persons-years"). The latter is useful because it lets researchers compare the instantaneous rate of a disease’s spread even in disparate time periods (for example, an incidence of 14 per 1000 persons-years could mean 14 cases would be expected for 1000 persons observed for 1 year, or 50 persons observed for 20 years). The only caveat to this use of incidence is the assumption that the rate will always be linear over the period in question, so longer time periods are more susceptible to incidence errors.
Finally there is the reproduction ratio, which is a measure of how many people each infected person will spread the disease to before they recover. In order for a disease to spread at all that ratio has to be greater than 1 (such that each infected person infects at least one more person). Up to now the ratios estimated for H1N1 Swine flu have been between 1.4 and 1.6. Recently, however, researchers at the National Institute of Health and Medical Research in Paris have re-estimated the ratio using some different assumptions and found it to be between 2.2 and 3.1 in Mexico, well within the range of numbers required for a pandemic. With the recent report of 135 new cases of H1N1 in Japan, the World Health Organization still denies an official pandemic is underway but evidence is mounting that H1N1 may have a higher incidence than previously thought.
For more information:
http://blogs.sciencemag.org/scienceinsider/2009/05/swine-flus-rate.html
http://blogs.sciencemag.org/scienceinsider/2009/05/h1n1-rocks-japa.html
http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=19205
© A Quantum of Science / Peter Smalley (2009)
Reproduction with attribution is appreciation
First let's tackle the jargon.
Prevalence is the total number of cases of a disease or infection in a given population. The important thing to remember about prevalence is that it is all the cases, not just the new ones, so the longer it takes to recover from a particular infection, the higher the prevalence will be. Most of the H1N1 figures you hear or read about are prevalence numbers, and as such are not as accurate a reflection as they might be.
Incidence is the rate at which new cases occur in a population, and is a better measure of how fast a disease is spreading because it takes out the duration-of-illness factor included in prevalence. Incidence is usually reported per capita ("3 new infections per 1000 people") or even with a time-element ("14 per 1000 persons-years"). The latter is useful because it lets researchers compare the instantaneous rate of a disease’s spread even in disparate time periods (for example, an incidence of 14 per 1000 persons-years could mean 14 cases would be expected for 1000 persons observed for 1 year, or 50 persons observed for 20 years). The only caveat to this use of incidence is the assumption that the rate will always be linear over the period in question, so longer time periods are more susceptible to incidence errors.
Finally there is the reproduction ratio, which is a measure of how many people each infected person will spread the disease to before they recover. In order for a disease to spread at all that ratio has to be greater than 1 (such that each infected person infects at least one more person). Up to now the ratios estimated for H1N1 Swine flu have been between 1.4 and 1.6. Recently, however, researchers at the National Institute of Health and Medical Research in Paris have re-estimated the ratio using some different assumptions and found it to be between 2.2 and 3.1 in Mexico, well within the range of numbers required for a pandemic. With the recent report of 135 new cases of H1N1 in Japan, the World Health Organization still denies an official pandemic is underway but evidence is mounting that H1N1 may have a higher incidence than previously thought.
For more information:
http://blogs.sciencemag.org/scienceinsider/2009/05/swine-flus-rate.html
http://blogs.sciencemag.org/scienceinsider/2009/05/h1n1-rocks-japa.html
http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=19205
© A Quantum of Science / Peter Smalley (2009)
Reproduction with attribution is appreciation
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