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Authors: Laurie Garrett
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Researchers also understood that viruses had a variety of different types of proteins protruding from their capsules, most of which were used by the tiny microbes to lock on to cells and gain entry for invasion. Some of the most sophisticated viruses, such as influenza, sugarcoated those proteins so that the human immune system might fail to notice the disguised invaders.
In 1963 laboratory scientists knew they could also distinguish one virus species from another by testing immune responses to those proteins protruding from the viral capsules. Humans and higher animals made antibodies against most such viral proteins, and the antibodiesâwhich were themselves large proteinsâwere very specific. Usually an antibody against parts of the polio virus, for example, would not react against the smallpox virus. Indeed, some antibodies were so picky that they might react against a 1958 Chicago strain of the flu, but not the strain that hit the Windy City the following winter.
Jonas Salk used this response against outer capsule proteins of the polio virus as the basis of his revolutionary vaccine, and by 1963 medical and veterinary pioneers all over the world were finding the pieces of various viruses that could be used most effectively to raise human and animal antibody responses.
Back in the lab, they could also use antibody responses to find out what might be ailing a mysteriously ill person. Blood samples containing the victimâs attacking microbe would be dotted across a petri dish full of human or animal cells. Antibodies would also be dotted across the dish, and scientists would wait to see which antibody samples successfully prevented viral kill of the cells in the petri dish.
Of course, if the virus was something never before studied, all the scientists would be able to get was a negative answer: âItâs not anything that we know about, none of our antibodies work.â So in the face of something new, like Machupo, scientists could only say after a tedious process of antibody elimination, âWe donât know what it is.â
With bacteria the process of identification was far easier because the organisms were orders of magnitude larger than viruses: whereas a virus might be about one ten-millionth of an inch in size, a bacterium would be a thousandth of an inch long. To see a virus, scientists needed powerful, expensive electron microscopes, but since the days of Dutch lens hobbyist Anton van Leeuwenhoek, who in 1674 invented a microscope, it has been possible for people to see what he called âwee animalculesâ with little more than a well-crafted glass lens and candlelight.
The relationship between those âanimalculesâ and disease was first figured out by Franceâs Louis Pasteur in 1864, and during the following hundred years bacteriologists learned so much about the organisms that young scientists in 1964 considered classic bacteriology a dead field.
In 1928 British scientist Alexander Fleming had discovered that Penicillium mold could kill Staphylococcus bacteria in petri dishes, and dubbed the lethal antibacterial chemical secreted by the mold âpenicillin.â 13 In 1944 penicillin was introduced to general clinical practice, causing a worldwide sensation that would be impossible to overstate. The term âmiracle drugâ entered the common vernacular as parents all over the industrialized world watched their children bounce back immediately from ailments that just months before had been considered serious, even deadly. Strep throat, once a dreaded childhood disease, instantly became trivial, as did skin boils, infected wounds, and tuberculosis with the quick discovery of streptomycin and other classes of antibiotics. By 1965 more than 25,000 different antibiotic products had been developed; physicians and scientists felt that bacterial diseases, and the microbes responsible, were no longer of great concern or of research interest.
Amid the
Researchers also understood that viruses had a variety of different types of proteins protruding from their capsules, most of which were used by the tiny microbes to lock on to cells and gain entry for invasion. Some of the most sophisticated viruses, such as influenza, sugarcoated those proteins so that the human immune system might fail to notice the disguised invaders.
In 1963 laboratory scientists knew they could also distinguish one virus species from another by testing immune responses to those proteins protruding from the viral capsules. Humans and higher animals made antibodies against most such viral proteins, and the antibodiesâwhich were themselves large proteinsâwere very specific. Usually an antibody against parts of the polio virus, for example, would not react against the smallpox virus. Indeed, some antibodies were so picky that they might react against a 1958 Chicago strain of the flu, but not the strain that hit the Windy City the following winter.
Jonas Salk used this response against outer capsule proteins of the polio virus as the basis of his revolutionary vaccine, and by 1963 medical and veterinary pioneers all over the world were finding the pieces of various viruses that could be used most effectively to raise human and animal antibody responses.
Back in the lab, they could also use antibody responses to find out what might be ailing a mysteriously ill person. Blood samples containing the victimâs attacking microbe would be dotted across a petri dish full of human or animal cells. Antibodies would also be dotted across the dish, and scientists would wait to see which antibody samples successfully prevented viral kill of the cells in the petri dish.
Of course, if the virus was something never before studied, all the scientists would be able to get was a negative answer: âItâs not anything that we know about, none of our antibodies work.â So in the face of something new, like Machupo, scientists could only say after a tedious process of antibody elimination, âWe donât know what it is.â
With bacteria the process of identification was far easier because the organisms were orders of magnitude larger than viruses: whereas a virus might be about one ten-millionth of an inch in size, a bacterium would be a thousandth of an inch long. To see a virus, scientists needed powerful, expensive electron microscopes, but since the days of Dutch lens hobbyist Anton van Leeuwenhoek, who in 1674 invented a microscope, it has been possible for people to see what he called âwee animalculesâ with little more than a well-crafted glass lens and candlelight.
The relationship between those âanimalculesâ and disease was first figured out by Franceâs Louis Pasteur in 1864, and during the following hundred years bacteriologists learned so much about the organisms that young scientists in 1964 considered classic bacteriology a dead field.
In 1928 British scientist Alexander Fleming had discovered that Penicillium mold could kill Staphylococcus bacteria in petri dishes, and dubbed the lethal antibacterial chemical secreted by the mold âpenicillin.â 13 In 1944 penicillin was introduced to general clinical practice, causing a worldwide sensation that would be impossible to overstate. The term âmiracle drugâ entered the common vernacular as parents all over the industrialized world watched their children bounce back immediately from ailments that just months before had been considered serious, even deadly. Strep throat, once a dreaded childhood disease, instantly became trivial, as did skin boils, infected wounds, and tuberculosis with the quick discovery of streptomycin and other classes of antibiotics. By 1965 more than 25,000 different antibiotic products had been developed; physicians and scientists felt that bacterial diseases, and the microbes responsible, were no longer of great concern or of research interest.
Amid the
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