The Coming Plague (144 page)
Authors: Laurie Garrett
88
P. J. Cascone, T. F. Haydar, and A. E. Simon, “Sequences and Structures Required for Recombination Between Virus-Associated RNAs,” Science 260 (1993): 801â5.
89
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.
91
M. C. Y. Heny, S. Y. Heng, and S. G. Allen, “Co-Infection and Synergy of Human Immunodeficiency Virus-1 and Herpes Simplex Virus-1,”
Lancet
343 (1994): 255â58.
Lancet
343 (1994): 255â58.
92
D. Bartels,
New Scientist
, July 30, 1987: 53â54.
New Scientist
, July 30, 1987: 53â54.
93
L. Feigenbaum and G. Khoury, “The Role of Enhancer Elements in Viral Host Range and Pathogenicity,” in B. Fields, M. A. Martin, and D. Kamely, eds.,
Genetically Altered Viruses and the Environment
(New York: Cold Spring Harbor Laboratory, 1985).
Genetically Altered Viruses and the Environment
(New York: Cold Spring Harbor Laboratory, 1985).
94
B. N. Fields, D. M. Knipe, R. M. Chanock, et al.,
Virology
(New York: Raven Press, 1985).
Virology
(New York: Raven Press, 1985).
95
For a sense of the microbial ecology issues Fields felt constituted the mysterious “orchestration,” see M. L. Nibert, D. B. Furlong, and B. N. Fields, “Mechanisms of Viral Pathogenesis,”
Journal of Clinical Investigation
88 (1991): 727â34; A. Learmouth,
Disease Ecology
(New York: Basil Blackwell, 1988); and D. E. Pomeroy and M. W. Service, “The Ecology of Man,” Chapter 8 in
Tropical Ecology
(Essex, Eng.: Longman Scientific and Technical, 1986).
Journal of Clinical Investigation
88 (1991): 727â34; A. Learmouth,
Disease Ecology
(New York: Basil Blackwell, 1988); and D. E. Pomeroy and M. W. Service, “The Ecology of Man,” Chapter 8 in
Tropical Ecology
(Essex, Eng.: Longman Scientific and Technical, 1986).
96
J. D. Watson, N. H. Hopkins, J. W. Roberts, et al.,
Molecular Biology of the Gene
(4th ed.; Menlo Park, CA: Benjamin/Cummings, 1987).
Molecular Biology of the Gene
(4th ed.; Menlo Park, CA: Benjamin/Cummings, 1987).
97
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,
Mobile DNA
(Washington, D.C.: American Society for Microbiology, 1989).
Mobile DNA
(Washington, D.C.: American Society for Microbiology, 1989).
98
S. E. Luria and M. Delbruck, “Mutations of Bacteria from Virus Sensitivity to Virus Resistance,”
Genetics
28 (1943): 491â511; and J. Lederberg and E. M. Lederberg, “Replica Plating and Indirect Selection of Bacterial Mutants,”
Journal of Bacteriology
63 (1952): 399â406.
Genetics
28 (1943): 491â511; and J. Lederberg and E. M. Lederberg, “Replica Plating and Indirect Selection of Bacterial Mutants,”
Journal of Bacteriology
63 (1952): 399â406.
99
J. Cairns, J. Overbaugh, and S. Miller, “The Origin of Mutants,”
Nature
335 (1988): 142â46.
Nature
335 (1988): 142â46.
100
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
P. L. Foster, “
Escherichia coli and Salmonella typhirium
, Mutagenesis,”
Encyclopedia of Microbiology
3 (1992): 1â8.
Escherichia coli and Salmonella typhirium
, Mutagenesis,”
Encyclopedia of Microbiology
3 (1992): 1â8.
102
R. I. Morimoto, “Cells in Stress: Transcriptional Activation of Heat Shock Genes,”
Science
259 (1993): 1409â10.
Science
259 (1993): 1409â10.
103
C. T. Walsh, “Vancomycin Resistance: Decoding the Molecular Logic,”
Science
261 (1993): 308â9.
Science
261 (1993): 308â9.
104
S. P. Cohen, W. Yan, and S. B. Levy, “A Multidrug Resistance Regulation Chromosomal Locus Is Widespread Among Enteric Bacteria,”
Journal of Infectious Diseases
168 (1993): 484â88.
Journal of Infectious Diseases
168 (1993): 484â88.
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
169 (1994): 119â26.
Escherichia coli
Strains Causing Urosepsis,”
Journal of Infectious Diseases
169 (1994): 119â26.
106
J. Travis, “Possible Evolutionary Role Explored for âJumping Genes,'”
Science
257 (1992): 884â85.
Science
257 (1992): 884â85.
107
A. A. Beaudry and G. F. Joyce, “Directed Evolution of an RNA Enzyme,”
Science
257 (1992): 635â41.
Science
257 (1992): 635â41.
108
R. E. Lenski and J. E. Mittler, “The Directed Mutational Controversy and Neo-Darwinism,”
Science
259 (1993): 188â93.
Science
259 (1993): 188â93.
109
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
173 (1991): 7471â80.
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
173 (1991): 7471â80.
112
D. R. Schaberg, “Evolution of Antimicrobial Resistance and Nosocomial Infection: Lessons from the Vanderbilt Experiment,”
American Journal of Medicine
70 (1981): 445â49; and C. F. Amabile-Cuevas and M. E. Chicurel, “Bacterial Plasmids and Gene Flux,”
Cell
70 (1992): 189â99.
American Journal of Medicine
70 (1981): 445â49; and C. F. Amabile-Cuevas and M. E. Chicurel, “Bacterial Plasmids and Gene Flux,”
Cell
70 (1992): 189â99.
113
S. Schwarz and S. GrolzâKrug, “The Cloramphenicol-Streptomycin-Resistance Plasmid from a Clinical Strain of
Staphylococcus sciuri
and Its Structural Relationship to Other Staphylococcal Resistance Plasmids,”
FEMS Microbiology Letters
66 (1991): 319â22; and T. J. Coffey, C. G. Dowson, M. Daniels, et al., “Horizontal Transfer of Multiple Penicillin-Binding Protein Genes, and Capsular Biosynthetic Genes, in Natural Populations of
Streptococcus pneumoniae,” Molecular Microbiology
5 (1991): 2255â60.
Staphylococcus sciuri
and Its Structural Relationship to Other Staphylococcal Resistance Plasmids,”
FEMS Microbiology Letters
66 (1991): 319â22; and T. J. Coffey, C. G. Dowson, M. Daniels, et al., “Horizontal Transfer of Multiple Penicillin-Binding Protein Genes, and Capsular Biosynthetic Genes, in Natural Populations of
Streptococcus pneumoniae,” Molecular Microbiology
5 (1991): 2255â60.
114
P. Viljanen and J. Boratynski, “The Susceptibility of Conjugative Resistance Transfer in Gram-Negative Bacteria to Physiochemical and Biochemical Agents,”
FEMS Microbiology Reviews
8 (1991): 43â54.
FEMS Microbiology Reviews
8 (1991): 43â54.
115
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
264 (1994): 258â60.
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
, November 17, 1986: 75â76; and A. S. Moffat, “Theoretical Ecology: Winning Its Spurs in the Real World,”
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
N. M. Ampel, “PlaguesâWhat's Past Is Present: Thoughts on the Origin and History of New Infectious Diseases,”
Review of Infectious Diseases
13 (1991): 658â65.
Review of Infectious Diseases
13 (1991): 658â65.
118
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.
119
P. W. Ewald,
Evolution of Infectious Disease
(New York: Oxford University Press, 1993).
Evolution of Infectious Disease
(New York: Oxford University Press, 1993).
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,”
Scientific American
(April 1993): 86â93.
Human Nature
2 (1990): 1â30; and P. W. Ewald, “The Evolution of Virulence,”
Scientific American
(April 1993): 86â93.
123
R. B. Johnson, “Human Disease and the Evolution of Pathogen Virulence,”
Journal of Theoretical Biology
122 (1986): 19â24; G. C. Williams and R. M. Neese, “The Dawn of Darwinian Medicine,”
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.
Journal of Theoretical Biology
122 (1986): 19â24; G. C. Williams and R. M. Neese, “The Dawn of Darwinian Medicine,”
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.
125
J. F. Miller, J. J. Mekalanos, and S. Falkow, “Coordinate Regulation and Sensory Transduction in the Control of Bacterial Virulence,”
Science
243 (1989): 916â22; C. Upton, K. Mossman,
and G. McFadden, “Encoding of a Homolog of the IFN-gamma Receptor by Myxoma Virus,”
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.
Science
243 (1989): 916â22; C. Upton, K. Mossman,
and G. McFadden, “Encoding of a Homolog of the IFN-gamma Receptor by Myxoma Virus,”
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
, March 30, 1988: 113â20.
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.
Other books
White As Snow (Fairy Tale) by Tanith Lee
MATCHED PEARLS by Grace Livingston Hill
Fear of Falling by Catherine Lanigan
Remember Tuesday Morning by Karen Kingsbury
Light in August by William Faulkner
Erotica Storytime #1 - Three Men and a Tiny Lady by Kiss, Tori
Who We Were Before by Leah Mercer
A Necklace of Water by Cate Tiernan
Love Forevermore by Madeline Baker
Savage Spring by Constance O'Banyon
