The Coming Plague (118 page)

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Authors: Laurie Garrett

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45
R. Dubos,
Mirage of Health: Utopias, Progress, and Biological Change
(Garden City, NY: Anchor Books, 1961), 138–39.
46
T. McKeown, R. G. Record, and R. D. Turner, “An Interpretation of the Decline of Mortality in England and Wales During the Twentieth Century,”
Population Studies
29 (1974): 391–422.
47
R. C. Baron, J. B. McCormick, and O. A. Zubeir, “Ebola Virus Disease in Southern Sudan: Hospital Dissemination and Intrafamilial Spread,”
Bulletin of the World Health Organization
61 (1983): 997–1003.
48
Time would prove McCormick sadly correct, as conditions in southern Sudan worsened steadily year by year. Widespread famine, over a decade of civil war, and massive refugee migrations would render the area a highly vulnerable ecology for the microbes. By mid-1993 the region would be suffering massive epidemics of AIDS, visceral leishmaniasis or kala-azar, tuberculosis, bacterial meningitis, a host of diarrheal diseases, leprosy, measles, and malaria. If Ebola and Marburg diseases were also rampant at that time they were undetectable, hidden under an overlay of so much disease that nearly every southern Sudanese seemed stricken by at least one potentially life-threatening ailment.
For further details, see
Leishmaniasis Epidemic in Southern Sudan
, WHO/6 (Geneva: World Health Organization, January 26, 1993); R. W. Ashford and M. C. Thomson, “Visceral Leishmaniasis in Sudan: A Delayed Development Disaster?”
Annals of Tropical Medicine and Parasitology
85 (1991): 571–72; W. A. Perea, T. Ancelle, A. Moren, et al., “Visceral Leishmaniasis in Southern Sudan,”
Transactions of the Royal Society of Tropical Medicine and Hygiene
85 (1991): 48–53; R. Rosenblatt, “The Last Place on Earth,”
Vanity Fair
, July 1993: 89–91, 114–20; and J. Seaman, D. Pryce, H. E. Sandorp, et al., “Epidemic Visceral Leishmaniasis in Sudan: A Randomized Trial of Aminosidine Plus Sodium Stibogluconate Versus Sodium Stiboglutinate Alone,”
Journal of Infectious Diseases
168 (1993): 715–19.
8. Revolution
1
J. D. Watson and F. H. C. Crick, “A Structure for Deoxyribonucleic Acid,”
Nature
171 (1953): 737.
2
There are many excellent resources for further information about recombinant DNA techniques. They include P. Berg and M. Singer,
Dealing with Genes: The Language of Heredity
(Mill Valley, CA: University Science Books, 1992); M. Singer and P. Berg,
Genes to Genomes
(Mill Valley, CA: University Science Books, 1991); and J. D. Watson, N. H. Hopkins, J. W. Roberts, et al.,
Molecular Biology of the Gene
(4th ed.; Menlo Park, CA: Benjamin/Cummings Publishing Co., 1987).
3
For an excellent review of McClintock's work and its subsequent impact on molecular biology, see N. V. Federoff, “Maize Transposable Elements.” Chapter 14 in D. E. Berg and M. M. Howe, eds.,
Mobile DNA
(Washington, D.C.: American Society for Microbiology, 1989). One of McClintock's seminal papers is B. McClintock, “The Origin and Behavior of Mutable Loci in Maize,”
Proceedings of the National Academy of Sciences
36 (1950): 344–55.
4
James Watson has written four editions of his grand guide to molecular biology, each of which, since the first in 1965, has been considerably larger than its predecessor, reflecting the explosion of scientific discovery. The most recent edition of
Molecular Biology of the Gene
, completed in 1987 (op. cit.), has this marvelous description of the mobile DNA phenomenon: “Moveable DNA segments called transposons occasionally jump around chromosomes, thus fundamentally altering chromosomal structure. In addition to neatly moving genes, transposons also scramble DNA, making deletions, inversions,
and other rearrangements. It is becoming clear that such changes are a critical feature of chromosome evolution, particularly in eucaryotic cells. We now appreciate that recombination is not accidental, but is instead an essential cellular process catalyzed by enzymes that cells encode and regulate for the purpose.”
5
D. Baltimore, “Retroviruses and Cancer,”
Hospital Practice
, January 1978: 49–57.
6
S. S. Morse, “Evolution, Viral,”
Encyclopedia of Microbiology,
Vol. 2 (New York: Academic Press, 1992), 141–55.
7
For an excellent list of key transposable elements in common use for genetic engineering, see C. M. Berg, D. E. Berg, and E. A. Groisman, “Transposable Elements and Genetic Engineering,” Chapter 41 in Berg and Howe, eds. (1989), op. cit.
8
J. M. Bishop, “Viruses, Genes, and Cancer,”
Harvey Lecture
, March 17, 1983.
9
D. H. Spector, H. E. Varmus, and J. M. Bishop, “Nucleotide Sequences Related to the Transforming Gene of Avian Sarcoma Virus Are Present in DNA of Uninfected Vertebrates,”
Proceedings of the National Academy of Sciences
75 (1978): 4102–06; and D. Stehelin, H. E. Varmus, J. M. Bishop, and P. K. Vogt, “DNA Related to the Transforming Gene(s) of Avian Sarcoma Viruses Is Present in Normal Avian DNA,”
Nature
260 (1976): 170–73.
10
Bishop (1983), op. cit.
11
J. M. Bishop, “Oncogenes,”
Scientific American
246 (1982): 80–92; and H. E. Varmus, “Form and Function of Retroviral Proviruses,”
Science
216 (1982): 812–20.
12
K. Takatsuki, T. Uchiyama, K. Sagawa, and J. Yodoi, in S. Seno, F. Takaku, and S. Irino, eds.,
Topics in Hematology
(Amsterdam: Excerpta Medica, 1977), 73–77.
13
Though the acronym HTLV would remain, Gallo—at the urging of numerous scientific colleagues—later changed the L in HTLV from “leukemia” to “lymphotropic,” reflecting increasing evidence that the virus rarely caused leukemia but always attacked lymphoid cells.
14
B. J. Poiesz, F. W. Ruscetti, M. Reitz, et al., “Isolation of a New Type C Retrovirus (HTLV) in Primary Uncultured Cells of a Patient with Sezary T-Cell Leukemia,”
Nature
294 (1981): 268–75.
15
Robert Gallo's version of these events appears in his 1991 book,
Virus Hunting—AIDS, Cancer, and the Human Retrovirus: A Story of Scientific Discovery
(New York: New Republic). The Japanese perspective has not been published. Also see B. J. Poiesz, F. W. Ruscetti, A. F. Gazdar, et al., “Detection and Isolation of Type-C Retrovirus Particles from Fresh and Cultured Lymphocytes of a Patient with Cutaneous T-Cell Lymphoma,”
Proceedings of the National Academy of Sciences
77 (1980): 7415–19.
16
I. Miyoshi, M. Fujishita, H. Taguchi, et al., “Natural Infection in Non-human Primates with Adult T-Cell Leukemia Virus or a Closely Related Agent,”
International Journal of Cancer
32 (1983): 333–36.
17
I. Miyoshi, S. Yoshimoto, M. Fujishita, et al., “Natural Adult T-Cell Leukemia Virus Infection in Japanese Monkeys,”
Lancet
II (1982): 658.
18
An interesting side note to this story concerns the ultimate fate of the MO line. It has always been difficult to grow normal human cells under laboratory conditions; nearly all studies are done on human cancer cells cloned from specific tumor lines because cancer cells will grow under all sorts of conditions, including inside glass tubes. These clones are given names and the cell lines are sold to researchers all over the world. Such a line, if proven free of contamination and relatively indicative of general human cell activity, can fetch good prices. Golde thought MO might prove a fantastic experimental cell line, and filed a U.S. patent petition. If granted a patent, he would be able to reap royalties from all MO sales to researchers worldwide and profit from any products derived from the cell line. Golde's plans backfired, however, when the patient, John Moore, a Seattle salesman, questioned Golde's right to patent his cells, which had been removed from his spleen. The issue became more heated as the profit potentials grew. Moore's MO cells were the source of the discovery of the immune system protein GM-CSF, as well as the HTLV-II virus, which greatly increased the value of the line. As of 1993 the dispute continued to wend its way through the American legal system, having grown extraordinarily complex. A good review of the MO controversy appeared in J. Stone, “Cells for Sale,”
Discover
, August 1988: 33–39.
19
J. S. Y. Chen, J. McLaughlin, J. C. Garson, et al., “Molecular Characterization of Genome of a Novel Human T-Cell Leukaemia Virus,”
Nature
305 (1983): 502–5.
20
V. S. Kalyanaraman, M. G. Sarngadharan, M. Robert-Guroff, et al., “A New Subtype of Human T-cell Leukemia Virus (HTLV-II) Associated with a T-cell Variant of Hairy Cell Leukemia,”
Science
218 (1982): 571–73.
21
A good example of the public perspective at the time can be found in Larry Agran's
The Cancer Connection and What We Can Do About It
(Boston: Houghton Mifflin, 1977). Agran asserted that “we can change the man-made environment that causes 90 percent of all human cancer.”
22
G. Hunsmann, J. Schneider, J. Schmitt, and N. Yamamoto, “Detection of Serum Antibodies to Adult T-Cell Leukemia Virus in Non-Human Primates and in People from Africa,”
International Journal of Cancer
32 (1983): 329–32.
23
K. Yamaguchi, “Human T-Lymphotropic Virus Type I in Japan,”
Lancet
343 (1994): 213–16.
24
By 1994 Brooklyn, New York, would be an HTLV-I epicenter, due to its sizable Caribbean immigrant population. See N. S. Larsen, “Study Confirms High Rates of Adult T-Cell Leukemia in N. Y. C.,”
Jonrnal of the National Cancer Institute
86 (1994): 85–86.
25
F. A. Vyth-Dreese, P. Rumke, M. Robert-Guroff, et al., “Antibodies Against Human T-Cell Leukemia/Lymphoma Virus in Relatives of a T-Cell Leukemia Patient Originating from Surinam,”
International Journal of Cancer
32 (1983): 337–42.
26
V. Manzari, A. Gradilone, G. Barillari, et al., “HTLV-I Is Endemic in Southern Italy: Detection of the First Infectious Cluster in a White Population,”
International Journal of Cancer
36 (1985): 557–59.
27
Gallo (1991), op. cit.; “Call It Ishmael,”
Hospital Practice
, September 15, 1985: 29; and Z. Ben-Ishai, “Human T-Cell Lymphotropic Virus Type-1 Antibodies in Falashas and Other Ethnic Groups in Israel,”
Nature
315 (1985): 665.
28
A. F. Fleming, “HTLV from Africa to Japan,”
Lancet
I (1984): 279.
29
W. F. H. Jarrett, E. M. Crawford, W. B. Martin, and F. Davie, “Leukemia in the Cat: A Virus-like Particle Associated with Leukaemia (Lymphosarcoma),”
Nature
202 (1964): 567. W. D. Hardy, Jr., L. J. Old, P. W. Hess, et al., “Horizontal Transmission of Feline Leukaemia Virus,”
Nature
244 (1973): 266–69; and D. P. Francis, M. Essex, and W. D. Hardy, Jr., “Excretion of Feline Leukemia Virus by Naturally Infected Pet Cats,”
Nature
269 (1977): 252–54. M. Essex, G. Klein, S. P. Snyder, and J. B. Harrold, “Correlation Between Humoral Antibody and Regression of Tumours Induced by Feline Sarcoma Virus,”
Nature
233 (1971): 195–96. M. Essex, W. D. Hardy, Jr., S. M. Cotter, et al., “Naturally Occurring Persistent Feline Oncornavirus Infections in the Absence of Disease,”
Infection and Immunology
11 (1975): 470–75; and M. Essex, A. Sliski, S. M. Cotter, et al., “Immuno-surveillance of Naturally Occurring Feline Leukemia,”
Science
190 (1975): 790–92.
30
The lab's interest in hepatitis B reflected Don Francis's stay, which was briefly interrupted in 1976 by his work on Ebola in Sudan. The hepatitis B virus was discovered in 1965, and shown to cause liver cancer in 1978. See W. Szmuness, “Hepatocellular Carcinoma and the Hepatitis B Virus: Evidence for a Causal Association,”
Progress in Medical Virology
24 (1978): 40–69. Francis planned to set up hepatitis B surveillance around the United States when he returned to the CDC in an effort to determine just how many Americans suffered from tumors caused by the virus. His scientific thinking about hepatitis B was described in D. P. Francis, M. Essex, and J. E. Mynard, “Feline Leukemia Virus and Hepatitis B Virus: A Comparison of Late Manifestations,”
Progress in Medical Virology
27 (1981): 127–32.
31
M. Essex, “Adult T-Cell Leukemia-Lymphoma: Role of a Human Retrovirus,”
Journal of the National Cancer lnstitute
69 (1982): 981–85.
32
J. Summers, J. M. Smolec, and R. Snyder, “A Virus Similar to Human Hepatitis B Virus Associated with Hepatitis and Hepatoma in Woodchucks,”
Proceedings of the National Academy of Sciences
75 (1978): 4533–37.
33
Forty-fifth World Assembly, “Implementation of the Global Strategy for Health for All by the Year 2000, Second Evaluation; and Eighth Report on the World Health Situation” (Geneva: World Health Organization, 1992), 10.
34
D. Burkitt, “A Lymphoma Syndrome in Tropical Africa,”
International Review of Experimental Pathology
2 (1963): 67.
35
M. A. Epstein, B. G. Achong, and Y. M. Barr, “Virus Particles in Cultured Lymphoblasts from Burkitt's Lymphoma,”
Lancet
II (1964): 702.
36
G. Orth, F. Breitburd, M. Faure, and O. Croissant, “Papilloma-virus: A Possible Role in Human Cancer,” in H. H. Hiatt, J. D. Watson, and J. A. Winsten, eds.,
Origins of Human Cancer
(New York: Cold Spring Harbor Laboratory, 1977).

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