The Coming Plague (144 page)
Authors: Laurie Garrett
88
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Hypervariable regions were also found in human DNA. For example, in 1992â94 scientists working separately in laboratories all over the world made the exciting discovery that human DNA contained stretches of long repetitive sequences of what seemed to be garbage. Three nucleotides, such as a CTG, would be repeated over and over, up to fifty or sixty times. For unknown reasons, some people's cells would suddenly expand those repeats, up to 200 or more CTGs, and diseases would occur. Fragile-X Syndrome (Down's Syndrome), Huntington's Disease, Myotonic Dystrophy, and Spinobulbar Muscular Atrophy were all clearly linked to such triple-repeat regions of DNA. There were indications that Alzheimer's Disease was also a triple-repeat disorder.
90
This is the work of Ron Montelaro at Louisiana State University, often in collaboration with Jim Mullins, at Stanford University.
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See, for example, J. W. Ajioka and D. L. Hartl, “Population Dynamics of Transposable Elements,” Chapter 43 in D. E. Berg and M. M. Howe,
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Nature
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A key counterargument came also from Harvardâthe rival Medical School. Researchers showed that
E. coli
which carried an advantageous mutation could take over an apparently stagnant population of bacteria under stress. In their experiment, stressing a colony of bacteria caused the genetically advantaged to replace those that died without changing the overall size of the population. The researchers argued that Cairns and other supporters of the notion that bacteria could selectively mutate under stress were misinterpreting their results; randomness, they argued, was still at play, simply well disguised. See M. M. Zambrano, D. A. Siegele, M. Almirón, et al., “Microbial Competition:
Escherichia coli
Mutants That Take Over Stationary Phase Cultures,”
Science
259 (1993): 1757â58.
E. coli
which carried an advantageous mutation could take over an apparently stagnant population of bacteria under stress. In their experiment, stressing a colony of bacteria caused the genetically advantaged to replace those that died without changing the overall size of the population. The researchers argued that Cairns and other supporters of the notion that bacteria could selectively mutate under stress were misinterpreting their results; randomness, they argued, was still at play, simply well disguised. See M. M. Zambrano, D. A. Siegele, M. Almirón, et al., “Microbial Competition:
Escherichia coli
Mutants That Take Over Stationary Phase Cultures,”
Science
259 (1993): 1757â58.
101
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Journal of Infectious Diseases
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105
J. R. Johnson, I. Orskov, F. Orskov, et al., “0, K, and H Antigens Predict Virulence Factors, Carboxylesterase B Pattern, Antimicrobial Resistance, and Host Compromise Among
Escherichia coli
Strains Causing Urosepsis,”
Journal of Infectious Diseases
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Escherichia coli
Strains Causing Urosepsis,”
Journal of Infectious Diseases
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Science
257 (1992): 884â85.
Science
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Science
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Science
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R. E. Lenski and J. E. Mittler, “The Directed Mutational Controversy and Neo-Darwinism,”
Science
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Science
259 (1993): 188â93.
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D. A. Watson, “Unusual Mutational Mechanisms and Evolution,” Letter,
Science
260 (1993): 1958.
Science
260 (1993): 1958.
110
L. D. Hurst, “Unusual Mutational Mechanisms and Evolution,” Letter,
Science
260 (1993): 1959.
Science
260 (1993): 1959.
111
D. W. Hecht, T. J. Jagielo, and M. H. Malamy, “Conjugal Transfer of Antibiotic Resistance Factors in
Bacteroides fragilis
: The btgA and btgB Genes of Plasmid pBFTM10 Are Required for Its Transfer from
Bacteroides fragilis
and for Its Mobilization by IncP Beta Plasmid R751 in
Escherichia coli,” Journal of Bacteriology
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Bacteroides fragilis
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Bacteroides fragilis
and for Its Mobilization by IncP Beta Plasmid R751 in
Escherichia coli,” Journal of Bacteriology
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D. S. Thaler, “The Evolution of Genetic Intelligence,”
Science
264 (1994): 224â25; and R. S. Harris, S. Longerich, and S. M. Rosenberg, “Recombination in Adaptive Mutation,”
Science
264 (1994): 258â60.
Science
264 (1994): 224â25; and R. S. Harris, S. Longerich, and S. M. Rosenberg, “Recombination in Adaptive Mutation,”
Science
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116
See, for example, R. Levins, T. Awerbach, U. Brinkmann, et al., “The Emergence of New Diseases,”
American Scientist
82 (1994): 52â60; A. Gibbons, “Where Are âNew Diseases' Born?”
Science
261 (1993): 680â81; K. McAuliffe, “How New Are Today's New Diseases?”
U.S. News & World Report
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Science
263 (1994): 1090â92.
American Scientist
82 (1994): 52â60; A. Gibbons, “Where Are âNew Diseases' Born?”
Science
261 (1993): 680â81; K. McAuliffe, “How New Are Today's New Diseases?”
U.S. News & World Report
, November 17, 1986: 75â76; and A. S. Moffat, “Theoretical Ecology: Winning Its Spurs in the Real World,”
Science
263 (1994): 1090â92.
117
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Review of Infectious Diseases
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P. J. Kanki, K. U. Travers, S. MBoup, et al., “Slower Heterosexual Spread of HIV-2 Than HIV-1,”
Lancet
343 (1994): 943â96; and K. M. DeCock, G. Adjarlolo, E. Ekpini, et al., “Epidemiology and Transmission of HIV-2. Why There Is No HIV-2 Pandemic,”
Journal of the American Medical Association
270 (1993): 2083â86.
Lancet
343 (1994): 943â96; and K. M. DeCock, G. Adjarlolo, E. Ekpini, et al., “Epidemiology and Transmission of HIV-2. Why There Is No HIV-2 Pandemic,”
Journal of the American Medical Association
270 (1993): 2083â86.
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P. W. Ewald,
Evolution of Infectious Disease
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Evolution of Infectious Disease
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120
In Robert Gallo's lab at the National Cancer Institute researchers showed in 1990 that mixing different HIV-1 quasispecies and a mouse retrovirus resulted in an expansion of the range of cell types the viruses were able to infect, suggesting that the various viral strains swapped useful genes. See P. Lusso, M. di Veronese, B. Ensoli, et al., “Expanded HIV-1 Cellular Tropism by Phenotypic Mixing with Murine Endogenous Retroviruses,”
Science
247 (1990): 848â52.
Science
247 (1990): 848â52.
121
R. M. Anderson, R. M. May, M. C. Boily, et al., “The Spread of HIV-1 in Africa: Sexual Contact Patterns and the Predicted Demographic Impact of AIDS,”
Nature
352 (1991): 581â89.
Nature
352 (1991): 581â89.
122
P. W. Ewald, “Transmission Modes and the Evolution of Virulence,”
Human Nature
2 (1990): 1â30; and P. W. Ewald, “The Evolution of Virulence,”
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R. B. Johnson, “Human Disease and the Evolution of Pathogen Virulence,”
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106 (1991): 83â119.
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The Quarterly Review of Biology
66 (1991): 1â22; P. W. Ewald, “Pathogen-Induced Cycling of Outbreak Insect Populations,” Chapter 11 in
Insect Outbreaks
(New York: Academic Press, 1987); and P. W. Ewald, “Waterborne Transmission and the Evolution of Virulence Among Gastrointestinal Bacteria,”
Epidemiology of Infection
106 (1991): 83â119.
124
E. A. Herre, “Population Structure and the Evolution of Virulence in Nematode Parasites of Fig Wasps,”
Science
259 (1993): 1442â45.
Science
259 (1993): 1442â45.
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243 (1989): 916â22; C. Upton, K. Mossman,
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168 (1993): 961â68.
Science
243 (1989): 916â22; C. Upton, K. Mossman,
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Science
258 (1992): 1369â72; and L. E. Bermudez, L. S. Young, J. Martinelli, and M. Petrofsky, “Exposure to Ethanol Up-Regulates the Expression of
Mycobacteriam avium
Complex Proteins Associated with Bacterial Virulence,”
Journal of Infectious Diseases
168 (1993): 961â68.
126
See, for example, P. L. C. Small, L. Ramakrishnan, and S. Falkow, “Remodeling Schemes of Intracellular Pathogens,”
Science
263 (1994): 637â39; A. McMichael, “Natural Selection at Work on the Surface of Virus-Infected Cells,”
Science
260 (1993): 1771â72; S. Gupta, K. Trenholme, R. M. Anderson, and K. P. Day, “Antigenic Diversity of
Plasmodium falciparum,” Science
163 (1994): 961â63; W. W. Stead, “Genetics and Resistance to Tuberculosis,”
Anaals of Internal Medicine
116 (1992): 937â41; and M. Barinaga, “Viruses Launch Their Own 'âStar Wars,'”
Science
258 (1992): 1730â31.
Science
263 (1994): 637â39; A. McMichael, “Natural Selection at Work on the Surface of Virus-Infected Cells,”
Science
260 (1993): 1771â72; S. Gupta, K. Trenholme, R. M. Anderson, and K. P. Day, “Antigenic Diversity of
Plasmodium falciparum,” Science
163 (1994): 961â63; W. W. Stead, “Genetics and Resistance to Tuberculosis,”
Anaals of Internal Medicine
116 (1992): 937â41; and M. Barinaga, “Viruses Launch Their Own 'âStar Wars,'”
Science
258 (1992): 1730â31.
127
T. H. Weller, “Science, Society, and Changing Viral-Host Relationships,”
Hospital Practice
, March 30, 1988: 113â20.
Hospital Practice
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128
A. Learmouth,
Patterns of Disease and Hunger
(Vancouver, BC: David and Charles, 1978); and P. R. Epstein, “Commentary: Pestilence and PovertyâHistorical Transitions and the Great Pandemics,”
American Journal of Preventative Medicine
8 (1992): 263â65.
Patterns of Disease and Hunger
(Vancouver, BC: David and Charles, 1978); and P. R. Epstein, “Commentary: Pestilence and PovertyâHistorical Transitions and the Great Pandemics,”
American Journal of Preventative Medicine
8 (1992): 263â65.
129
It is this factâ
that vaccines can't prevent infection
âwhich poses the greatest challenge to scientists who are trying to develop an AIDS vaccine. Since the AIDS virus gets inside cells of the immune system and hides for years on end inside human DNA with close to 100 percent lethal results, no level of infection can be acceptable. To date, no one has conceived of a vaccine that will prevent infection with any known microbe.
that vaccines can't prevent infection
âwhich poses the greatest challenge to scientists who are trying to develop an AIDS vaccine. Since the AIDS virus gets inside cells of the immune system and hides for years on end inside human DNA with close to 100 percent lethal results, no level of infection can be acceptable. To date, no one has conceived of a vaccine that will prevent infection with any known microbe.
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