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Re: [evol-psych] remade by virus

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  • james kohl
    Excerpted from below: With increased crowding and air travel putting us at risk, Crawford wonders whether we might ever conquer microbes completely, and
    Message 1 of 6 , Feb 3, 2013
    • 0 Attachment
      Excerpted from below: "With increased crowding and air travel putting us at risk, Crawford wonders whether we might ever conquer microbes completely, and whether we need a more microbe-centric view of the world."

      My comment:
      A more microbe-centric view includes the fact that adaptive evolution is nutrient-dependent and pheromone-controlled in species from microbes to man. The apparent danger to us all is random mutations theory, since it is an enabler for theorists who like to tell stories that have no basis in biological fact.

      For contrast, Greg Bear included the HERV effect as an explanation for evolution of a new species of humans who communicated their species' difference via pheromones. He took what he called "the next logical step" more than a decade ago, which led to his presentation in 2004 to the American Philosophical Society.

      Is Bear a forward-thinking research scientist with academic credentials and superior insight into the molecular biology of adaptive evolution? No! He's a novelist who makes more sense in two science fiction novels than evolutionary theorists have made in more than 150 years. See for example: When Genes Go Walkabout: "Neural networks from beehives to brains solve problems through the exchange and the selective cancellation and modification of signals." The signals, of course, are nutrient-dependent hormones and pheromones.

      I wonder how much longer it will be until others begin to comment on how ridiculous random mutations theory is -- and always has been. It would be great to hear from others who take the time to educate themselves after reading the news article Anna posted, and minimally, these abstracts. Evidently, we're not going to hear from the theorists until all this blows over -- if ever the biological facts do that.

      Differences in HERV-K LTR insertions in orthologous loci of humans and great apes

      Human-Specific HERV-K Intron LTRs Have Nonaccidental Opposite Orientation Relative to the Direction of Gene Transcription and Might Be Involved in the Antisense Regulation of Gene Expression

       
      James V. Kohl
      Medical laboratory scientist (ASCP)
      Independent researcher
      Kohl, J.V. (2012) Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. Socioaffective Neuroscience & Psychology, 2: 17338.



      From: Anna <pantheon@...>
      To: 4DWorldx@yahoogroups.com
      Sent: Sat, February 2, 2013 11:22:33 PM
      Subject: [evol-psych] remade by virus

       

      "The Virus Planet" -- Earth's Invisible World Would Reach Out 100-Million Light Years (Weekend Feature)

       

      Posted: 02 Feb 2013 06:53 AM PST


      Nile Delta at Night


      In the invisible, parallel world of Earth's they kill half the bacteria in the ocean every day, and invade a microbe host 10 trillion times a second around the world. There are 10 billion trillion, trillion viruses inhabiting Planet Earth, which is more stars than are in the Universe -- stacked end to end, they would reach out 100 million light years.

      Over tens, hundreds and millions years, our ancestors have been picking up retroviruses (HIV is a retrovirus) that reproduce by taking their genetic material and inserting it into our own chromosomes. There are probably about 100,000 elements in the human genome that you can trace to a virus ancestor. They make up about 8 percent of our genome, and genes that encode proteins only make up 1.2 percent of our genome making us more virus than human.
      Occasionally, a retrovirus will end up in a sperm cell or an egg and insert its genes there, which then may give rise to a new organism, a new animal, a new person where every cell in that body has got that virus.

      In 2009, MIT researchers have explained why two mutations in the H1N1 avian flu virus were critical for viral transmission in humans during the 1918 pandemic outbreak that killed at least 50 million people -- believed more than that taken by the Black Death, and higher than the number killed in World War I.

      The 1918 flu pandemic -- commonly known as the Spanish flu -- was an influenza pandemic that started in the United States, appeared in West Africa and France and then spread to nearly every part of the globe in three waves lasting from March 1918 to June 1920, spreading to the Arctic and remote Pacific islands. It was caused by an unusually severe and deadly Influenza A virus strain of subtype H1N1.

      In contrast to most influenza outbreaks which predominantly affect juvenile, elderly, or otherwise weakened patients, the Spanish Flu also claimed healthy young adults, resulting from infection rates of up to 50% and the extreme severity of the symptoms, suspected to be caused by cytokine storms.

      6a00d8341bf7f753ef01538f14c7a8970b-500wi

      The disease was first discovered at Fort Riley, Kansasand Queens, New York , in 1918. In August 1918, a more virulent strain appeared simultaneously in Brest, France, in West Africa at Freetown, Sierra Leone, and in the U.S. at Boston, Massachusetts. The Allies of World War I came to call it the Spanish Flu, primarily because the pandemic received greater press attention after it moved from France to Spain in November of 1918.

      The MIT team showed that the 1918 influenza strain developed two mutations in a surface molecule called hemagglutinin (HA), which allowed it to bind tightly to receptors in the human upper respiratory tract.

      259-Spanish-flu

      Fast forward to the apst few years, with the reports of a massive outbreak of E. coli in Europe, which seemed to fit the pattern: people were infected with E. coli apparently after eating contaminated vegetables. But when German hospitals sent samples of the E. coli to the Beijing Genome Center on June 2, 2011 to have their DNA sequenced, the Chinese researchers reported that the strain was not the same E. coli that contaminated the spinach, known as O157:H7.

      In fact, it was an entirely different strain of E. coli, called O104:H4, that had never been associated with epidemics. Somehow this obscure microbe had turned savage, triggering one of the biggest — if not the biggest— E. coli epidemics in history, with at least 1,730 infections and 18 deaths to date.
      “We didn’t know this bug was out there,” said Phillip Tarr, a microbiologist at
      Washington State University in an interview with Newsweek.

      What makes these outbreaks particularly confusing, reports Carl Zimmer, author of The Rise of Superbacteria, is that E. coli is, for the most part, a harmless creature. We are each home to billions of harmless E. coli that inhabit our intestines.

      "But in the mid-1900s," writes Zimmer, "scientists began uncovering strains of E. coli that could cause life-threatening diarrhea. Unlike ordinary E. coli, they carried genes for a poison known as Shiga toxin, named for Japanese bacteriologist Kiyoshi Shiga. Over time, microbiologists identified a number of strains of disease-causing bacteria, classifying them by the proteins on their surface.

      In 1982, E. coli O157:H7 burst on the scene with particularly grisly flair. It struck 25 people in Medford, Ore., and then three months later the same strain caused an outbreak in Traverse City, Mich. Scientists were able to trace the bacteria back to undercooked hamburgers."

      Scientists have found a half dozen other strains that cause similar illnesses, but E. coli O157:H7 has been responsible for the lion’s share of E. coli food poisoning, striking again in 1993 in contaminated hamburgers in Washington state, for example, sickening 732 people and killing four of them. But it has not used just hamburger to infect its victims. Along with the spinach outbreak of 2006, E. coli O157:H7 has turned up in lettuce, bean sprouts, and even cookie dough.

      A deadly new strain of E. coli has spread fear across Europe about meat and vegatables.The sudden debut of E. coli O157:H7 in the 1980s made many people wonder how it had come to be. Was it the monstrous product of the modern food industry? Tarr and his colleagues analyzed the genome of the bacteria to estimate its time of origin.

      “These organisms have been around for 7,000 years,” says Tarr. It’s possible that E. coli O157:H7 and other pathogenic strains caused outbreaks for centuries before microbiologists could identify them as the cause.

      A look at the genetic makeup of E. coli O157:H7 is cause for even more concern. It evolved into a deadly pathogen by picking up genes from other bacteria through a process called recombination. Viruses, for example, can move from one E. coli to another and insert genes from their old host into a new one. “E. coli are a cauldron of recombination,” says Tarr.

      The European strain did not belong to any of these well-known suspects. Initially, it appeared that the bacteria were coming from cucumbers and other vegetables from organic farms in Spain, but O104:H4 has not turned up in tests at those places. Researchers are now left to wonder where exactly it came from.

      The O104:H4 genome sequence suggests that it’s yet another concoction from evolution’s brew. The bacteria contain many segments of DNA not seen in other E. coli strains, writes Zimmer.

      "This new DNA may be responsible for its high level of virulence—more than a quarter of victims went on to develop the dangerous form of the disease," he added "The O104:H4 strain has even acquired new genes that make them resistant to antibiotics. As a result, doctors have few options to treat the bacteria. In Germany, physicians are resorting to an experimental antibody treatment to see if it can help."

      “Microbes are always going to be one step ahead of us. Their generation time is 24 hours, ours is 30 years. They mutate, they change, they will find a way. They are amazing opportunists,” writes Dorothy Crawford, Professor of Medical Microbiology at the University of Edinburgh and author ofDeadly Companions.

      Microbes have evolved with us over the millennia, shaping human civilization through infection, disease, and deadly pandemic. Beginning with a dramatic account of the SARS pandemic at the start of the 21st century, As our move from hunter-gatherer to farmer to city-dweller accelerated, we became ever more vulnerable to microbe attack.

      With increased crowding and air travel putting us at risk, Crawford wonders whether we might ever conquer microbes completely, and whether we need a more microbe-centric view of the world.

      The Daily Galaxy via
      Newsweek.com, npr.org and carlzimmer.com

      Image credit Spanish Flu Virus: Courtesy, Yoshihiro Kawaoka, University of Wisconsin-Madison

    • james kohl
      Excerpted from below: With increased crowding and air travel putting us at risk, Crawford wonders... whether we need a more microbe-centric view of the
      Message 2 of 6 , Feb 3, 2013
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        Excerpted from below: "With increased crowding and air travel putting us at risk, Crawford wonders... whether we need a more microbe-centric view of the world.


        My blog-post from 11/22/10


        In his book "Darwin's Radio" (1999, Del Rey) and his sequel "Darwin's Children" (2003, Del Rey), science fiction author and novelist Greg Bear successfully predicted that human endogenous retroviruses are involved in human speciation. His new subspecies of humans communicated with pheromones, as do other species from yeasts to non-human primates. This example of science fiction becoming fact contributes to a scientific understanding of epigenetics and human pheromones via a forward-thinking author's grasp of molecular biology and his willingness to take the next logical step for his readers. Other fictional representations of human pheromones must also have some basis in fact; enough to be included on Wikipedia and other informative sources, if only to encourage forward-thinking by others. Indeed, in his November 2003 presentation before the American Philosophical Society, Greg Bear said: "What we [science fiction writers] write is far from authoritative, or final, but science fiction works best when it stimulates debate." Moving forward as he spoke about epigenetic influences, he also said that chemical signals between organisms can change genetic expression. This allows the social environment to modify gene expression in individuals and in their offspring.


        More than a decade has passed since Bear’s conceptualization of how pheromones might exert a powerful epigenetic influence on other species and on us. Those who are familiar with current works from molecular biology can now more fully recognize that Greg Bear was at least a decade ahead of his time. For example, see this article on human endogenous retroviruses and primate speciation. Also, my co-authors and I wrote about epigenetic influences and pheromones in 1996. The take home message that’s available through the integration of science fiction and scientific fact is that pheromones may be the most significant epigenetic influence of all. We are beginning to see this more clearly after our species sequenced the human genome and as we learn more about epigenetic facts predicted by Bear's science fiction.

         
        James V. Kohl
        Medical laboratory scientist (ASCP)
        Independent researcher
        Kohl, J.V. (2012) Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. Socioaffective Neuroscience & Psychology, 2: 17338.



        From: Anna <pantheon@...>
        To: 4DWorldx@yahoogroups.com
        Sent: Sat, February 2, 2013 11:22:33 PM
        Subject: [evol-psych] remade by virus

         

        "The Virus Planet" -- Earth's Invisible World Would Reach Out 100-Million Light Years (Weekend Feature)

         

        Posted: 02 Feb 2013 06:53 AM PST


        Nile Delta at Night


        In the invisible, parallel world of Earth's they kill half the bacteria in the ocean every day, and invade a microbe host 10 trillion times a second around the world. There are 10 billion trillion, trillion viruses inhabiting Planet Earth, which is more stars than are in the Universe -- stacked end to end, they would reach out 100 million light years.

        Over tens, hundreds and millions years, our ancestors have been picking up retroviruses (HIV is a retrovirus) that reproduce by taking their genetic material and inserting it into our own chromosomes. There are probably about 100,000 elements in the human genome that you can trace to a virus ancestor. They make up about 8 percent of our genome, and genes that encode proteins only make up 1.2 percent of our genome making us more virus than human.
        Occasionally, a retrovirus will end up in a sperm cell or an egg and insert its genes there, which then may give rise to a new organism, a new animal, a new person where every cell in that body has got that virus.

        In 2009, MIT researchers have explained why two mutations in the H1N1 avian flu virus were critical for viral transmission in humans during the 1918 pandemic outbreak that killed at least 50 million people -- believed more than that taken by the Black Death, and higher than the number killed in World War I.

        The 1918 flu pandemic -- commonly known as the Spanish flu -- was an influenza pandemic that started in the United States, appeared in West Africa and France and then spread to nearly every part of the globe in three waves lasting from March 1918 to June 1920, spreading to the Arctic and remote Pacific islands. It was caused by an unusually severe and deadly Influenza A virus strain of subtype H1N1.

        In contrast to most influenza outbreaks which predominantly affect juvenile, elderly, or otherwise weakened patients, the Spanish Flu also claimed healthy young adults, resulting from infection rates of up to 50% and the extreme severity of the symptoms, suspected to be caused by cytokine storms.

        6a00d8341bf7f753ef01538f14c7a8970b-500wi

        The disease was first discovered at Fort Riley, Kansasand Queens, New York , in 1918. In August 1918, a more virulent strain appeared simultaneously in Brest, France, in West Africa at Freetown, Sierra Leone, and in the U.S. at Boston, Massachusetts. The Allies of World War I came to call it the Spanish Flu, primarily because the pandemic received greater press attention after it moved from France to Spain in November of 1918.

        The MIT team showed that the 1918 influenza strain developed two mutations in a surface molecule called hemagglutinin (HA), which allowed it to bind tightly to receptors in the human upper respiratory tract.

        259-Spanish-flu

        Fast forward to the apst few years, with the reports of a massive outbreak of E. coli in Europe, which seemed to fit the pattern: people were infected with E. coli apparently after eating contaminated vegetables. But when German hospitals sent samples of the E. coli to the Beijing Genome Center on June 2, 2011 to have their DNA sequenced, the Chinese researchers reported that the strain was not the same E. coli that contaminated the spinach, known as O157:H7.

        In fact, it was an entirely different strain of E. coli, called O104:H4, that had never been associated with epidemics. Somehow this obscure microbe had turned savage, triggering one of the biggest — if not the biggest— E. coli epidemics in history, with at least 1,730 infections and 18 deaths to date.
        “We didn’t know this bug was out there,” said Phillip Tarr, a microbiologist at
        Washington State University in an interview with Newsweek.

        What makes these outbreaks particularly confusing, reports Carl Zimmer, author of The Rise of Superbacteria, is that E. coli is, for the most part, a harmless creature. We are each home to billions of harmless E. coli that inhabit our intestines.

        "But in the mid-1900s," writes Zimmer, "scientists began uncovering strains of E. coli that could cause life-threatening diarrhea. Unlike ordinary E. coli, they carried genes for a poison known as Shiga toxin, named for Japanese bacteriologist Kiyoshi Shiga. Over time, microbiologists identified a number of strains of disease-causing bacteria, classifying them by the proteins on their surface.

        In 1982, E. coli O157:H7 burst on the scene with particularly grisly flair. It struck 25 people in Medford, Ore., and then three months later the same strain caused an outbreak in Traverse City, Mich. Scientists were able to trace the bacteria back to undercooked hamburgers."

        Scientists have found a half dozen other strains that cause similar illnesses, but E. coli O157:H7 has been responsible for the lion’s share of E. coli food poisoning, striking again in 1993 in contaminated hamburgers in Washington state, for example, sickening 732 people and killing four of them. But it has not used just hamburger to infect its victims. Along with the spinach outbreak of 2006, E. coli O157:H7 has turned up in lettuce, bean sprouts, and even cookie dough.

        A deadly new strain of E. coli has spread fear across Europe about meat and vegatables.The sudden debut of E. coli O157:H7 in the 1980s made many people wonder how it had come to be. Was it the monstrous product of the modern food industry? Tarr and his colleagues analyzed the genome of the bacteria to estimate its time of origin.

        “These organisms have been around for 7,000 years,” says Tarr. It’s possible that E. coli O157:H7 and other pathogenic strains caused outbreaks for centuries before microbiologists could identify them as the cause.

        A look at the genetic makeup of E. coli O157:H7 is cause for even more concern. It evolved into a deadly pathogen by picking up genes from other bacteria through a process called recombination. Viruses, for example, can move from one E. coli to another and insert genes from their old host into a new one. “E. coli are a cauldron of recombination,” says Tarr.

        The European strain did not belong to any of these well-known suspects. Initially, it appeared that the bacteria were coming from cucumbers and other vegetables from organic farms in Spain, but O104:H4 has not turned up in tests at those places. Researchers are now left to wonder where exactly it came from.

        The O104:H4 genome sequence suggests that it’s yet another concoction from evolution’s brew. The bacteria contain many segments of DNA not seen in other E. coli strains, writes Zimmer.

        "This new DNA may be responsible for its high level of virulence—more than a quarter of victims went on to develop the dangerous form of the disease," he added "The O104:H4 strain has even acquired new genes that make them resistant to antibiotics. As a result, doctors have few options to treat the bacteria. In Germany, physicians are resorting to an experimental antibody treatment to see if it can help."

        “Microbes are always going to be one step ahead of us. Their generation time is 24 hours, ours is 30 years. They mutate, they change, they will find a way. They are amazing opportunists,” writes Dorothy Crawford, Professor of Medical Microbiology at the University of Edinburgh and author ofDeadly Companions.

        Microbes have evolved with us over the millennia, shaping human civilization through infection, disease, and deadly pandemic. Beginning with a dramatic account of the SARS pandemic at the start of the 21st century, As our move from hunter-gatherer to farmer to city-dweller accelerated, we became ever more vulnerable to microbe attack.

        With increased crowding and air travel putting us at risk, Crawford wonders whether we might ever conquer microbes completely, and whether we need a more microbe-centric view of the world.

        The Daily Galaxy via
        Newsweek.com, npr.org and carlzimmer.com

        Image credit Spanish Flu Virus: Courtesy, Yoshihiro Kawaoka, University of Wisconsin-Madison

      • Richard Ruquist
        James, I just read an article that suggests that our immune system needs microbes to be happy. Otherwise it will turn on itself. So in the last 50 years or so
        Message 3 of 6 , Feb 3, 2013
        • 0 Attachment
          James,

          I just read an article that suggests that our immune system needs microbes to be happy. Otherwise it will turn on itself.

          So in the last 50 years or so as the environment has become more and more sterile, the prevalence of auto-immune disease has increased. Is that believable?
          Richard

          On Sun, Feb 3, 2013 at 7:11 AM, james kohl <jvkohl@...> wrote:
           

          Excerpted from below: "With increased crowding and air travel putting us at risk, Crawford wonders whether we might ever conquer microbes completely, and whether we need a more microbe-centric view of the world."

          My comment:
          A more microbe-centric view includes the fact that adaptive evolution is nutrient-dependent and pheromone-controlled in species from microbes to man. The apparent danger to us all is random mutations theory, since it is an enabler for theorists who like to tell stories that have no basis in biological fact.

          For contrast, Greg Bear included the HERV effect as an explanation for evolution of a new species of humans who communicated their species' difference via pheromones. He took what he called "the next logical step" more than a decade ago, which led to his presentation in 2004 to the American Philosophical Society.

          Is Bear a forward-thinking research scientist with academic credentials and superior insight into the molecular biology of adaptive evolution? No! He's a novelist who makes more sense in two science fiction novels than evolutionary theorists have made in more than 150 years. See for example: When Genes Go Walkabout: "Neural networks from beehives to brains solve problems through the exchange and the selective cancellation and modification of signals." The signals, of course, are nutrient-dependent hormones and pheromones.

          I wonder how much longer it will be until others begin to comment on how ridiculous random mutations theory is -- and always has been. It would be great to hear from others who take the time to educate themselves after reading the news article Anna posted, and minimally, these abstracts. Evidently, we're not going to hear from the theorists until all this blows over -- if ever the biological facts do that.

          Differences in HERV-K LTR insertions in orthologous loci of humans and great apes

          Human-Specific HERV-K Intron LTRs Have Nonaccidental Opposite Orientation Relative to the Direction of Gene Transcription and Might Be Involved in the Antisense Regulation of Gene Expression

           
          James V. Kohl
          Medical laboratory scientist (ASCP)
          Independent researcher
          Kohl, J.V. (2012) Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. Socioaffective Neuroscience & Psychology, 2: 17338.



          From: Anna <pantheon@...>
          To: 4DWorldx@yahoogroups.com
          Sent: Sat, February 2, 2013 11:22:33 PM
          Subject: [evol-psych] remade by virus

           

          "The Virus Planet" -- Earth's Invisible World Would Reach Out 100-Million Light Years (Weekend Feature)

           

          Posted: 02 Feb 2013 06:53 AM PST


          Nile Delta at Night


          In the invisible, parallel world of Earth's they kill half the bacteria in the ocean every day, and invade a microbe host 10 trillion times a second around the world. There are 10 billion trillion, trillion viruses inhabiting Planet Earth, which is more stars than are in the Universe -- stacked end to end, they would reach out 100 million light years.

          Over tens, hundreds and millions years, our ancestors have been picking up retroviruses (HIV is a retrovirus) that reproduce by taking their genetic material and inserting it into our own chromosomes. There are probably about 100,000 elements in the human genome that you can trace to a virus ancestor. They make up about 8 percent of our genome, and genes that encode proteins only make up 1.2 percent of our genome making us more virus than human.
          Occasionally, a retrovirus will end up in a sperm cell or an egg and insert its genes there, which then may give rise to a new organism, a new animal, a new person where every cell in that body has got that virus.

          In 2009, MIT researchers have explained why two mutations in the H1N1 avian flu virus were critical for viral transmission in humans during the 1918 pandemic outbreak that killed at least 50 million people -- believed more than that taken by the Black Death, and higher than the number killed in World War I.

          The 1918 flu pandemic -- commonly known as the Spanish flu -- was an influenza pandemic that started in the United States, appeared in West Africa and France and then spread to nearly every part of the globe in three waves lasting from March 1918 to June 1920, spreading to the Arctic and remote Pacific islands. It was caused by an unusually severe and deadly Influenza A virus strain of subtype H1N1.

          In contrast to most influenza outbreaks which predominantly affect juvenile, elderly, or otherwise weakened patients, the Spanish Flu also claimed healthy young adults, resulting from infection rates of up to 50% and the extreme severity of the symptoms, suspected to be caused by cytokine storms.

          6a00d8341bf7f753ef01538f14c7a8970b-500wi

          The disease was first discovered at Fort Riley, Kansasand Queens, New York , in 1918. In August 1918, a more virulent strain appeared simultaneously in Brest, France, in West Africa at Freetown, Sierra Leone, and in the U.S. at Boston, Massachusetts. The Allies of World War I came to call it the Spanish Flu, primarily because the pandemic received greater press attention after it moved from France to Spain in November of 1918.

          The MIT team showed that the 1918 influenza strain developed two mutations in a surface molecule called hemagglutinin (HA), which allowed it to bind tightly to receptors in the human upper respiratory tract.

          259-Spanish-flu

          Fast forward to the apst few years, with the reports of a massive outbreak of E. coli in Europe, which seemed to fit the pattern: people were infected with E. coli apparently after eating contaminated vegetables. But when German hospitals sent samples of the E. coli to the Beijing Genome Center on June 2, 2011 to have their DNA sequenced, the Chinese researchers reported that the strain was not the same E. coli that contaminated the spinach, known as O157:H7.

          In fact, it was an entirely different strain of E. coli, called O104:H4, that had never been associated with epidemics. Somehow this obscure microbe had turned savage, triggering one of the biggest — if not the biggest— E. coli epidemics in history, with at least 1,730 infections and 18 deaths to date.
          “We didn’t know this bug was out there,” said Phillip Tarr, a microbiologist at
          Washington State University in an interview with Newsweek.

          What makes these outbreaks particularly confusing, reports Carl Zimmer, author of The Rise of Superbacteria, is that E. coli is, for the most part, a harmless creature. We are each home to billions of harmless E. coli that inhabit our intestines.

          "But in the mid-1900s," writes Zimmer, "scientists began uncovering strains of E. coli that could cause life-threatening diarrhea. Unlike ordinary E. coli, they carried genes for a poison known as Shiga toxin, named for Japanese bacteriologist Kiyoshi Shiga. Over time, microbiologists identified a number of strains of disease-causing bacteria, classifying them by the proteins on their surface.

          In 1982, E. coli O157:H7 burst on the scene with particularly grisly flair. It struck 25 people in Medford, Ore., and then three months later the same strain caused an outbreak in Traverse City, Mich. Scientists were able to trace the bacteria back to undercooked hamburgers."

          Scientists have found a half dozen other strains that cause similar illnesses, but E. coli O157:H7 has been responsible for the lion’s share of E. coli food poisoning, striking again in 1993 in contaminated hamburgers in Washington state, for example, sickening 732 people and killing four of them. But it has not used just hamburger to infect its victims. Along with the spinach outbreak of 2006, E. coli O157:H7 has turned up in lettuce, bean sprouts, and even cookie dough.

          A deadly new strain of E. coli has spread fear across Europe about meat and vegatables.The sudden debut of E. coli O157:H7 in the 1980s made many people wonder how it had come to be. Was it the monstrous product of the modern food industry? Tarr and his colleagues analyzed the genome of the bacteria to estimate its time of origin.

          “These organisms have been around for 7,000 years,” says Tarr. It’s possible that E. coli O157:H7 and other pathogenic strains caused outbreaks for centuries before microbiologists could identify them as the cause.

          A look at the genetic makeup of E. coli O157:H7 is cause for even more concern. It evolved into a deadly pathogen by picking up genes from other bacteria through a process called recombination. Viruses, for example, can move from one E. coli to another and insert genes from their old host into a new one. “E. coli are a cauldron of recombination,” says Tarr.

          The European strain did not belong to any of these well-known suspects. Initially, it appeared that the bacteria were coming from cucumbers and other vegetables from organic farms in Spain, but O104:H4 has not turned up in tests at those places. Researchers are now left to wonder where exactly it came from.

          The O104:H4 genome sequence suggests that it’s yet another concoction from evolution’s brew. The bacteria contain many segments of DNA not seen in other E. coli strains, writes Zimmer.

          "This new DNA may be responsible for its high level of virulence—more than a quarter of victims went on to develop the dangerous form of the disease," he added "The O104:H4 strain has even acquired new genes that make them resistant to antibiotics. As a result, doctors have few options to treat the bacteria. In Germany, physicians are resorting to an experimental antibody treatment to see if it can help."

          “Microbes are always going to be one step ahead of us. Their generation time is 24 hours, ours is 30 years. They mutate, they change, they will find a way. They are amazing opportunists,” writes Dorothy Crawford, Professor of Medical Microbiology at the University of Edinburgh and author ofDeadly Companions.

          Microbes have evolved with us over the millennia, shaping human civilization through infection, disease, and deadly pandemic. Beginning with a dramatic account of the SARS pandemic at the start of the 21st century, As our move from hunter-gatherer to farmer to city-dweller accelerated, we became ever more vulnerable to microbe attack.

          With increased crowding and air travel putting us at risk, Crawford wonders whether we might ever conquer microbes completely, and whether we need a more microbe-centric view of the world.

          The Daily Galaxy via
          Newsweek.com, npr.org and carlzimmer.com

          Image credit Spanish Flu Virus: Courtesy, Yoshihiro Kawaoka, University of Wisconsin-Madison


        • james kohl
          From: Richard Ruquist James, I just read an article that suggests that our immune system needs microbes to be happy. Otherwise it will turn on itself. So in
          Message 4 of 6 , Feb 3, 2013
          • 0 Attachment
            From: Richard Ruquist
            James,

            I just read an article that suggests that our immune system needs microbes to be happy. Otherwise it will turn on itself.

            So in the last 50 years or so as the environment has become more and more sterile, the prevalence of auto-immune disease has increased. Is that believable?


            JK: Minimally, it's an interesting correlate, especially in the context of antibiotic use with the side effect of peripheral neuropathy. My speculation is that killing the bacteria disrupts the continuity of the viral load, which helps to maintain systems-wide immune function that extends to the central nervous system and to the peripheral nervous system. I doubt that the manufacturers of the antibiotics are going to investigate cause and effect.

            James V. Kohl
            Medical laboratory scientist (ASCP)
            Independent researcher
            Kohl, J.V. (2012) Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. Socioaffective Neuroscience & Psychology, 2: 17338.





            On Sun, Feb 3, 2013 at 7:11 AM, james kohl <jvkohl@...> wrote:

            Excerpted from below: "With increased crowding and air travel putting us at risk, Crawford wonders whether we might ever conquer microbes completely, and whether we need a more microbe-centric view of the world."

            My comment:
            A more microbe-centric view includes the fact that adaptive evolution is nutrient-dependent and pheromone-controlled in species from microbes to man. The apparent danger to us all is random mutations theory, since it is an enabler for theorists who like to tell stories that have no basis in biological fact.

            For contrast, Greg Bear included the HERV effect as an explanation for evolution of a new species of humans who communicated their species' difference via pheromones. He took what he called "the next logical step" more than a decade ago, which led to his presentation in 2004 to the American Philosophical Society.

            Is Bear a forward-thinking research scientist with academic credentials and superior insight into the molecular biology of adaptive evolution? No! He's a novelist who makes more sense in two science fiction novels than evolutionary theorists have made in more than 150 years. See for example: When Genes Go Walkabout: "Neural networks from beehives to brains solve problems through the exchange and the selective cancellation and modification of signals." The signals, of course, are nutrient-dependent hormones and pheromones.

            I wonder how much longer it will be until others begin to comment on how ridiculous random mutations theory is -- and always has been. It would be great to hear from others who take the time to educate themselves after reading the news article Anna posted, and minimally, these abstracts. Evidently, we're not going to hear from the theorists until all this blows over -- if ever the biological facts do that.

            Differences in HERV-K LTR insertions in orthologous loci of humans and great apes

            Human-Specific HERV-K Intron LTRs Have Nonaccidental Opposite Orientation Relative to the Direction of Gene Transcription and Might Be Involved in the Antisense Regulation of Gene Expression

            James V. Kohl
            Medical laboratory scientist (ASCP)
            Independent researcher
            Kohl, J.V. (2012) Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. Socioaffective Neuroscience & Psychology, 2: 17338.



            From: Anna <pantheon@...>
            To: 4DWorldx@yahoogroups.com
            Sent: Sat, February 2, 2013 11:22:33 PM
            Subject: [evol-psych] remade by virus

            "The Virus Planet" -- Earth's Invisible World Would Reach Out 100-Million Light Years (Weekend Feature)

            Posted: 02 Feb 2013 06:53 AM PST


            Nile Delta at Night


            In the invisible, parallel world of Earth's they kill half the bacteria in the ocean every day, and invade a microbe host 10 trillion times a second around the world. There are 10 billion trillion, trillion viruses inhabiting Planet Earth, which is more stars than are in the Universe -- stacked end to end, they would reach out 100 million light years.

            Over tens, hundreds and millions years, our ancestors have been picking up retroviruses (HIV is a retrovirus) that reproduce by taking their genetic material and inserting it into our own chromosomes. There are probably about 100,000 elements in the human genome that you can trace to a virus ancestor. They make up about 8 percent of our genome, and genes that encode proteins only make up 1.2 percent of our genome making us more virus than human.
            Occasionally, a retrovirus will end up in a sperm cell or an egg and insert its genes there, which then may give rise to a new organism, a new animal, a new person where every cell in that body has got that virus.

            In 2009, MIT researchers have explained why two mutations in the H1N1 avian flu virus were critical for viral transmission in humans during the 1918 pandemic outbreak that killed at least 50 million people -- believed more than that taken by the Black Death, and higher than the number killed in World War I.

            The 1918 flu pandemic -- commonly known as the Spanish flu -- was an influenza pandemic that started in the United States, appeared in West Africa and France and then spread to nearly every part of the globe in three waves lasting from March 1918 to June 1920, spreading to the Arctic and remote Pacific islands. It was caused by an unusually severe and deadly Influenza A virus strain of subtype H1N1.

            In contrast to most influenza outbreaks which predominantly affect juvenile, elderly, or otherwise weakened patients, the Spanish Flu also claimed healthy young adults, resulting from infection rates of up to 50% and the extreme severity of the symptoms, suspected to be caused by cytokine storms.

            6a00d8341bf7f753ef01538f14c7a8970b-500wi

            The disease was first discovered at Fort Riley, Kansasand Queens, New York , in 1918. In August 1918, a more virulent strain appeared simultaneously in Brest, France, in West Africa at Freetown, Sierra Leone, and in the U.S. at Boston, Massachusetts. The Allies of World War I came to call it the Spanish Flu, primarily because the pandemic received greater press attention after it moved from France to Spain in November of 1918.

            The MIT team showed that the 1918 influenza strain developed two mutations in a surface molecule called hemagglutinin (HA), which allowed it to bind tightly to receptors in the human upper respiratory tract.

            259-Spanish-flu

            Fast forward to the apst few years, with the reports of a massive outbreak of E. coli in Europe, which seemed to fit the pattern: people were infected with E. coli apparently after eating contaminated vegetables. But when German hospitals sent samples of the E. coli to the Beijing Genome Center on June 2, 2011 to have their DNA sequenced, the Chinese researchers reported that the strain was not the same E. coli that contaminated the spinach, known as O157:H7.

            In fact, it was an entirely different strain of E. coli, called O104:H4, that had never been associated with epidemics. Somehow this obscure microbe had turned savage, triggering one of the biggest — if not the biggest— E. coli epidemics in history, with at least 1,730 infections and 18 deaths to date.
            “We didn’t know this bug was out there,” said Phillip Tarr, a microbiologist at
            Washington State University in an interview with Newsweek.

            What makes these outbreaks particularly confusing, reports Carl Zimmer, author of The Rise of Superbacteria, is that E. coli is, for the most part, a harmless creature. We are each home to billions of harmless E. coli that inhabit our intestines.

            "But in the mid-1900s," writes Zimmer, "scientists began uncovering strains of E. coli that could cause life-threatening diarrhea. Unlike ordinary E. coli, they carried genes for a poison known as Shiga toxin, named for Japanese bacteriologist Kiyoshi Shiga. Over time, microbiologists identified a number of strains of disease-causing bacteria, classifying them by the proteins on their surface.

            In 1982, E. coli O157:H7 burst on the scene with particularly grisly flair. It struck 25 people in Medford, Ore., and then three months later the same strain caused an outbreak in Traverse City, Mich. Scientists were able to trace the bacteria back to undercooked hamburgers."

            Scientists have found a half dozen other strains that cause similar illnesses, but E. coli O157:H7 has been responsible for the lion’s share of E. coli food poisoning, striking again in 1993 in contaminated hamburgers in Washington state, for example, sickening 732 people and killing four of them. But it has not used just hamburger to infect its victims. Along with the spinach outbreak of 2006, E. coli O157:H7 has turned up in lettuce, bean sprouts, and even cookie dough.

            A deadly new strain of E. coli has spread fear across Europe about meat and vegatables.The sudden debut of E. coli O157:H7 in the 1980s made many people wonder how it had come to be. Was it the monstrous product of the modern food industry? Tarr and his colleagues analyzed the genome of the bacteria to estimate its time of origin.

            “These organisms have been around for 7,000 years,” says Tarr. It’s possible that E. coli O157:H7 and other pathogenic strains caused outbreaks for centuries before microbiologists could identify them as the cause.

            A look at the genetic makeup of E. coli O157:H7 is cause for even more concern. It evolved into a deadly pathogen by picking up genes from other bacteria through a process called recombination. Viruses, for example, can move from one E. coli to another and insert genes from their old host into a new one. “E. coli are a cauldron of recombination,” says Tarr.

            The European strain did not belong to any of these well-known suspects. Initially, it appeared that the bacteria were coming from cucumbers and other vegetables from organic farms in Spain, but O104:H4 has not turned up in tests at those places. Researchers are now left to wonder where exactly it came from.

            The O104:H4 genome sequence suggests that it’s yet another concoction from evolution’s brew. The bacteria contain many segments of DNA not seen in other E. coli strains, writes Zimmer.

            "This new DNA may be responsible for its high level of virulence—more than a quarter of victims went on to develop the dangerous form of the disease," he added "The O104:H4 strain has even acquired new genes that make them resistant to antibiotics. As a result, doctors have few options to treat the bacteria. In Germany, physicians are resorting to an experimental antibody treatment to see if it can help."

            “Microbes are always going to be one step ahead of us. Their generation time is 24 hours, ours is 30 years. They mutate, they change, they will find a way. They are amazing opportunists,” writes Dorothy Crawford, Professor of Medical Microbiology at the University of Edinburgh and author ofDeadly Companions.

            Microbes have evolved with us over the millennia, shaping human civilization through infection, disease, and deadly pandemic. Beginning with a dramatic account of the SARS pandemic at the start of the 21st century, As our move from hunter-gatherer to farmer to city-dweller accelerated, we became ever more vulnerable to microbe attack.

            With increased crowding and air travel putting us at risk, Crawford wonders whether we might ever conquer microbes completely, and whether we need a more microbe-centric view of the world.

            The Daily Galaxy via
            Newsweek.com, npr.org and carlzimmer.com

            Image credit Spanish Flu Virus: Courtesy, Yoshihiro Kawaoka, University of Wisconsin-Madison


          • Edgar Owen
            Richard, Sounds like a reasonable theory. What s the evidence? Edgar
            Message 5 of 6 , Feb 3, 2013
            • 0 Attachment
              Richard,

              Sounds like a reasonable theory. What's the evidence?

              Edgar



              On Feb 3, 2013, at 9:47 AM, Richard Ruquist wrote:

              > James,
              >
              > I just read an article that suggests that our immune system needs microbes
              > to be happy. Otherwise it will turn on itself.
              >
              > So in the last 50 years or so as the environment has become more and more
              > sterile, the prevalence of auto-immune disease has increased. Is that
              > believable?
              > Richard
              >
              > On Sun, Feb 3, 2013 at 7:11 AM, james kohl <jvkohl@...> wrote:
              >
              >> **
              >>
              >>
              >> *Excerpted from below*: "With increased crowding and air travel putting
              >> us at risk, Crawford wonders whether we might ever conquer microbes
              >> completely, and whether we need a more microbe-centric view of the world."
              >> *
              >> My comment:* A more microbe-centric view includes the fact that adaptive
              >> evolution is nutrient-dependent and pheromone-controlled in species from
              >> microbes to man. The apparent danger to us all is random mutations theory,
              >> since it is an enabler for theorists who like to tell stories that have no
              >> basis in biological fact.
              >>
              >> For contrast, Greg Bear included the HERV effect as an explanation for
              >> evolution of a new species of humans who communicated their species'
              >> difference via pheromones. He took what he called "the next logical step"
              >> more than a decade ago, which led to his presentation in 2004 to the
              >> American Philosophical Society.
              >>
              >> Is Bear a forward-thinking research scientist with academic credentials
              >> and superior insight into the molecular biology of adaptive evolution? No!
              >> He's a novelist who makes more sense in two science fiction novels than
              >> evolutionary theorists have made in more than 150 years. See for example: When
              >> Genes Go Walkabout<http://www.amphilsoc.org/sites/default/files/480305.pdf>:
              >> "Neural networks from beehives to brains solve problems through the
              >> exchange and the selective cancellation and modification of signals." The
              >> signals, of course, are nutrient-dependent hormones and pheromones.
              >>
              >> I wonder how much longer it will be until others begin to comment on how
              >> ridiculous random mutations theory is -- and always has been. It would be
              >> great to hear from others who take the time to educate themselves after
              >> reading the news article Anna posted, and minimally, these abstracts.
              >> Evidently, we're not going to hear from the theorists until all this blows
              >> over -- if ever the biological facts do that.
              >>
              >> Differences in HERV-K LTR insertions in orthologous loci of humans and
              >> great apes<http://www.sciencedirect.com/science/article/B6T39-402KBCD-Y/2/c15a78cdd4f2999d3a8f374f8c8f7d69>
              >>
              >> Human-Specific HERV-K Intron LTRs Have Nonaccidental Opposite Orientation
              >> Relative to the Direction of Gene Transcription and Might Be Involved in
              >> the Antisense Regulation of Gene Expression<http://dx.doi.org/10.1023/A:1022294906202>
              >>
              >>
              >> James V. Kohl
              >> Medical laboratory scientist (ASCP)
              >> Independent researcher
              >> Kohl, J.V. (2012) Human pheromones and food odors: epigenetic influences
              >> on the socioaffective nature of evolved behaviors.<http://dx.doi.org/10.3402/snp.v2i0.17338>Socioaffective Neuroscience & Psychology, 2: 17338.
              >>
              >>
              >> ------------------------------
              >> *From:* Anna <pantheon@...>
              >> *To:* 4DWorldx@yahoogroups.com
              >> *Sent:* Sat, February 2, 2013 11:22:33 PM
              >> *Subject:* [evol-psych] remade by virus
              >>
              >>
              >>
              >> "The Virus Planet" -- Earth's Invisible World Would Reach Out
              >> 100-Million Light Years (Weekend Feature)<http://feedproxy.google.com/~r/TheDailyGalaxyNewsFromPlanetEarthBeyond/~3/w4USc4k-nVs/the-virus-planet-earths-invisible-world-that-would-reach-out-100-million-light-years-weekend-feature.html?utm_source=feedburner&utm_medium=email>
              >>
              >>
              >>
              >> Posted: 02 Feb 2013 06:53 AM PST
              >>
              >>
              >> [image: Nile Delta at Night]<http://www.dailygalaxy.com/.a/6a00d8341bf7f753ef0168e867796f970c-pi>
              >>
              >>
              >> In the invisible, parallel world of Earth's they kill half the bacteria in
              >> the ocean every day, and invade a microbe host 10 trillion times a second
              >> around the world. There are 10 billion trillion, trillion viruses
              >> inhabiting Planet Earth <http://en.wikipedia.org/wiki/Earth>, which is
              >> more stars than are in the Universe -- stacked end to end, they would reach
              >> out 100 million light years.
              >> Over tens, hundreds and millions years, our ancestors have been picking up
              >> retroviruses (HIV is a retrovirus) that reproduce by taking their genetic
              >> material and inserting it into our own chromosomes. There are probably
              >> about 100,000 elements in the human genome that you can trace to a virus
              >> ancestor. *They make up about 8 percent of our genome, and genes that
              >> encode proteins only make up 1.2 percent of our genome making us more virus
              >> than human. *
              >> *Occasionally, a retrovirus will end up in a sperm cell or an egg and
              >> insert its genes there, which then may give rise to a new organism, a new
              >> animal, a new person where every cell in that body has got that virus.*
              >>
              >> In 2009, MIT researchers have explained why two mutations in the H1N1
              >> avian flu virus were critical for viral transmission in humans during the
              >> 1918 pandemic outbreak that killed at least 50 million people -- believed
              >> more than that taken by the Black Death, and higher than the number killed
              >> in World War I.
              >>
              >> The 1918 flu pandemic -- commonly known as the Spanish flu<http://en.wikipedia.org/wiki/1918_flu_pandemic>-- was an influenza pandemic that started in the United States, appeared in
              >> West Africa and France and then spread to nearly every part of the globe in
              >> three waves lasting from March 1918 to June 1920, spreading to the Arctic
              >> and remote Pacific islands. It was caused by an unusually severe and deadly
              >> Influenza A virus strain of subtype H1N1.
              >>
              >> In contrast to most influenza outbreaks which predominantly affect
              >> juvenile, elderly, or otherwise weakened patients, the Spanish Flu also
              >> claimed healthy young adults, resulting from infection rates of up to 50%
              >> and the extreme severity of the symptoms, suspected to be caused by
              >> cytokine storms.
              >>
              >> [image: 6a00d8341bf7f753ef01538f14c7a8970b-500wi]<http://www.dailygalaxy.com/.a/6a00d8341bf7f753ef0168e86784dc970c-pi>
              >>
              >> The disease was first discovered at Fort Riley, Kansasand Queens, New York
              >> , in 1918. In August 1918, a more virulent strain appeared simultaneously
              >> in Brest, France, in West Africa at Freetown, Sierra Leone, and in the U.S.
              >> at Boston, Massachusetts. The Allies of World War I came to call it the
              >> Spanish Flu, primarily because the pandemic received greater press
              >> attention after it moved from France to Spain in November of 1918.
              >>
              >> The MIT team showed that the 1918 influenza strain developed two mutations
              >> in a surface molecule called hemagglutinin (HA), which allowed it to bind
              >> tightly to receptors in the human upper respiratory tract.
              >>
              >> [image: 259-Spanish-flu]<http://www.dailygalaxy.com/.a/6a00d8341bf7f753ef01676365f3b8970b-pi>
              >>
              >> Fast forward to the apst few years, with the reports of a massive outbreak
              >> of E. coli in Europe, which seemed to fit the pattern: people were infected
              >> with E. coli apparently after eating contaminated vegetables. But when
              >> German hospitals sent samples of the E. coli to the Beijing Genome Center
              >> on June 2, 2011 to have their DNA sequenced, the Chinese researchers
              >> reported that the strain was not the same E. coli that contaminated the
              >> spinach, known as O157:H7.
              >>
              >> In fact, it was an entirely different strain of E. coli, called O104:H4,
              >> that had never been associated with epidemics. Somehow this obscure microbe
              >> had turned savage, triggering one of the biggest — if not the biggest— E.
              >> coli epidemics in history, with at least 1,730 infections and 18 deaths to
              >> date.
              >> “We didn’t know this bug was out there,” said Phillip Tarr, a
              >> microbiologist at Washington State University<http://maps.google.com/maps?ll=46.7252,-117.1596&spn=1.0,1.0&q=46.7252,-117.1596%20(Washington%20State%20University)&t=h>in an interview with Newsweek.
              >>
              >> What makes these outbreaks particularly confusing, reports Carl Zimmer,
              >> author of *The Rise of Superbacteria<http://en.wikipedia.org/wiki/Escherichia_coli>
              >> *, is that E. coli is, for the most part, a harmless creature. We are
              >> each home to billions of harmless E. coli that inhabit our intestines.
              >>
              >> "But in the mid-1900s," writes Zimmer, "scientists began uncovering
              >> strains of E. coli that could cause life-threatening diarrhea. Unlike
              >> ordinary E. coli, they carried genes for a poison known as Shiga toxin,
              >> named for Japanese bacteriologist Kiyoshi Shiga. Over time, microbiologists
              >> identified a number of strains of disease-causing bacteria, classifying
              >> them by the proteins on their surface.
              >>
              >> In 1982, E. coli O157:H7<http://en.wikipedia.org/wiki/Escherichia_coli_O157%3AH7>burst on the scene with particularly grisly flair. It struck 25 people in
              >> Medford, Ore., and then three months later the same strain caused an
              >> outbreak in Traverse City, Mich. Scientists were able to trace the bacteria
              >> back to undercooked hamburgers."
              >>
              >> Scientists have found a half dozen other strains that cause similar
              >> illnesses, but E. coli O157:H7 has been responsible for the lion’s share of
              >> E. coli food poisoning, striking again in 1993 in contaminated hamburgers
              >> in Washington state, for example, sickening 732 people and killing four of
              >> them. But it has not used just hamburger to infect its victims. Along with
              >> the spinach outbreak of 2006, E. coli O157:H7 has turned up in lettuce,
              >> bean sprouts, and even cookie dough.
              >>
              >> A deadly new strain of E. coli has spread fear across Europe about meat
              >> and vegatables.The sudden debut of E. coli O157:H7 in the 1980s made many
              >> people wonder how it had come to be. Was it the monstrous product of the
              >> modern food industry? Tarr and his colleagues analyzed the genome of the
              >> bacteria to estimate its time of origin.
              >>
              >> “These organisms have been around for 7,000 years,” says Tarr. It’s
              >> possible that E. coli O157:H7 and other pathogenic strains caused outbreaks
              >> for centuries before microbiologists could identify them as the cause.
              >>
              >> A look at the genetic makeup of E. coli O157:H7 is cause for even more
              >> concern. It evolved into a deadly pathogen by picking up genes from other
              >> bacteria through a process called recombination. Viruses, for example, can
              >> move from one E. coli to another and insert genes from their old host into
              >> a new one. “E. coli are a cauldron of recombination,” says Tarr.
              >>
              >> The European strain did not belong to any of these well-known suspects.
              >> Initially, it appeared that the bacteria were coming from cucumbers and
              >> other vegetables from organic farms in Spain, but O104:H4 has not turned up
              >> in tests at those places. Researchers are now left to wonder where exactly
              >> it came from.
              >>
              >> The O104:H4 genome sequence suggests that it’s yet another concoction from
              >> evolution’s brew. The bacteria contain many segments of DNA not seen in
              >> other E. coli strains, writes Zimmer.
              >>
              >> "This new DNA may be responsible for its high level of virulence—more than
              >> a quarter of victims went on to develop the dangerous form of the disease,"
              >> he added "The O104:H4 strain has even acquired new genes that make them
              >> resistant to antibiotics. As a result, doctors have few options to treat
              >> the bacteria. In Germany, physicians are resorting to an experimental
              >> antibody treatment to see if it can help."
              >>
              >> “Microbes are always going to be one step ahead of us. Their generation
              >> time is 24 hours, ours is 30 years. They mutate, they change, they will
              >> find a way. They are amazing opportunists,” writes Dorothy Crawford,
              >> Professor of Medical Microbiology at the University of Edinburgh and author
              >> of*Deadly Companions.*
              >>
              >> Microbes have evolved with us over the millennia, shaping human
              >> civilization through infection, disease, and deadly pandemic. Beginning
              >> with a dramatic account of the SARS pandemic at the start of the 21st
              >> century, As our move from hunter-gatherer to farmer to city-dweller
              >> accelerated, we became ever more vulnerable to microbe attack.
              >>
              >> With increased crowding and air travel putting us at risk, Crawford
              >> wonders whether we might ever conquer microbes completely, and whether we
              >> need a more microbe-centric view of the world.
              >>
              >> The Daily Galaxy via Newsweek.com<http://www.dailygalaxy.com/my_weblog/2012/03/www.newsweek.com>,
              >> npr.org <http://www.dailygalaxy.com/my_weblog/2012/03/www.npr.org> and
              >> carlzimmer.com<http://www.dailygalaxy.com/my_weblog/2012/03/www.carlzimmer.com>
              >>
              >> Image credit Spanish Flu Virus: Courtesy, Yoshihiro Kawaoka, University of
              >> Wisconsin-Madison
              >>
              >>
              >>
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