The Coming Plague (55 page)
Authors: Laurie Garrett
In 1982 Liebowitch put forward the hypothesis that AIDS was a viral disease of African origin that caused illness and death by, as he put it, “completely burning out the immune system.” He urged his French medical colleagues to scour recent records for bizarre immunodeficiency cases among African-born residents of France or among French citizens who had traveled or resided in Africa. He further asserted that the Haitian cases represented a Caribbean expression of the African phenomenon, linked somehow by travel between French-speaking African countries and Haiti.
In Belgium, Peter Piot was hard at work on a very similar hypothesis. From the moment he had heard of the first Los Angeles PCP cases, Piot had considered the possibility that AIDS was the culprit in similar ailments among African residents of Belgium. So had Dr. Nathan Clumeck, a low-key physician working in Brussels' St. Pierre University Hospital. In 1982â83 he was treating five upper-class Zairois who either lived in Belgium or had come to the former colonial power for treatment of their profound immunodeficiencies.
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Clearly these African cases veered strongly off the course of AIDS events defined by the Americans: none were gay, used injected narcotics, or had visited Haiti. And more than a third were women. All evidence indicated that AIDS had been recently imported to the European continent from Africa, Haiti, or the United States. The American importation centered on blood products and gay sexual transmissions, while the African and Haitian cases seemed to involve importation of a heterosexual pattern of the disease. Regardless of the mode of transmission, however, it all argued strongly for, as the French Groupe de travail put it, “a transmissible agent now present in Europe.”
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It was a heterosexually transmitted microbe as well as a homosexually transmitted one, the European doctors said. And most members of the Groupe de travail favored the notion that AIDS was a viral disease.
France didn't have an NIH-type financial bureaucracy for dispersal of scientific research funds. Rather, it had a somewhat more elitist system
that concentrated the bulk of the country's biomedical research inside the prestigious Pasteur Institute in Paris. Though the Pasteur could hardly compare in size or wealth with the vast American scientific establishment, it had a distinct advantage in an emergency: individual scientists with “tenure” could initiate research in nearly any direction without answering to a bureaucratic superstructure. Though this was less democratic than the American system, the Pasteur system did intentionally allow the nation's scientific elite tremendous creativity and flexibility. The leading Paris hospitalsâClaude Bernard, Raymond Poincaré, St. Louis, Pitié-Salpetriereâwere free to collaborate with the Pasteur Institute scientists. In 1982, then, a loose AIDS collaboration had developed connecting Dr. Françoise Brun-Vézinet of Claude Bernard Hospital, Willy Rozenbaum of Pitié-Salpetrière, and a Pasteur group headed by virologist Luc Montagnier.
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that concentrated the bulk of the country's biomedical research inside the prestigious Pasteur Institute in Paris. Though the Pasteur could hardly compare in size or wealth with the vast American scientific establishment, it had a distinct advantage in an emergency: individual scientists with “tenure” could initiate research in nearly any direction without answering to a bureaucratic superstructure. Though this was less democratic than the American system, the Pasteur system did intentionally allow the nation's scientific elite tremendous creativity and flexibility. The leading Paris hospitalsâClaude Bernard, Raymond Poincaré, St. Louis, Pitié-Salpetriereâwere free to collaborate with the Pasteur Institute scientists. In 1982, then, a loose AIDS collaboration had developed connecting Dr. Françoise Brun-Vézinet of Claude Bernard Hospital, Willy Rozenbaum of Pitié-Salpetrière, and a Pasteur group headed by virologist Luc Montagnier.
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On January 3, 1983, Rozenbaum removed an enlarged lymph node from the neck of AIDS patient Frédéric Brugière, a gay man who had traveled in the United States. The precious tissue was rushed to Montagnier's lab, where virologist Françoise Barré-Sinoussi began analyzing it. On January 25, Barré-Sinoussi told Montagnier she had discovered evidence of reverse-transcriptase activity in Brugière's cells.
Only one entity on the planet was known to use the reverse-transcriptase enzyme: retroviruses. The tiny RNA viruses used the enzyme to make mirror-image copies of their RNA genetic material, creating a DNA version of themselves that could be incorporated into the genes of the animal cells that they infected.
Two human retroviruses were known to exist at that timeâHTLV-I and HTLV-IIâand the bulk of the world's research on them was done at Robert Gallo's laboratory in the National Cancer Institute. Montagnier initially assumed that the reverse-transcriptase activity indicated that AIDS was caused by one of these two agents, and his laboratory notebook for January describes Barré-Sinoussi's finding under the later-scratched-out heading of “HTLV-I.”
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Montagnier telephoned Gallo in early February 1983, described Barré-Sinoussi's findings, and a tempestuous collaboration/competition between the two laboratories began. Later that month Gallo's lab also had reverse-transcriptase activity in laboratory isolates of cells extracted from men with AIDS.
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Gallo was thoroughly convinced that his initial insights, voiced the previous year in his fateful phone conversation with Max Essex, remained accurate: AIDS was caused either by HTLV-I or by one of its close cousins.
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Gallo was thoroughly convinced that his initial insights, voiced the previous year in his fateful phone conversation with Max Essex, remained accurate: AIDS was caused either by HTLV-I or by one of its close cousins.
“HTLV is endemic in the Caribbean and seems to be relatively common in Africa, and of course AIDS has some link with the Caribbean island of Haiti and with Kaposi's sarcoma found traditionally in Africa,” Gallo told the
Journal of the American Medical Association
in August 1983.
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Admitting that no cases of AIDS had appeared in Japan, where HTLV-I was
endemic, Gallo asked, “Could the leukemia-causing virus [HTLV-I] be a variant of the immunosuppressive virus? We don't know. But if it is, it's a very subtle variant with a minor antigenic difference.”
Journal of the American Medical Association
in August 1983.
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Admitting that no cases of AIDS had appeared in Japan, where HTLV-I was
endemic, Gallo asked, “Could the leukemia-causing virus [HTLV-I] be a variant of the immunosuppressive virus? We don't know. But if it is, it's a very subtle variant with a minor antigenic difference.”
While Gallo's and Montagnier's groups raced to find the HTLV link, Jay Levy's tiny team of scientists toiled away in San Francisco, backed by just a few thousand dollars from the recently organized California state-university-wide AIDS Task Force.
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Despite his meager resources, Levy had a key advantage over the Bethesda and Paris researchers: virtually unlimited access to a large and cooperative AIDS patient population. While Montagnier struggled with samples from one key patient, Gallo with a handful, Levy had blood and tissue samples from more than forty gay San Franciscans. His vast research pool let Levy select patients at random, avoiding any unintended biases that might result from overinterpreting data extrapolated from one or two patients. It would be several years before the importance of Levy's randomly selected samples would be obvious.
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Despite his meager resources, Levy had a key advantage over the Bethesda and Paris researchers: virtually unlimited access to a large and cooperative AIDS patient population. While Montagnier struggled with samples from one key patient, Gallo with a handful, Levy had blood and tissue samples from more than forty gay San Franciscans. His vast research pool let Levy select patients at random, avoiding any unintended biases that might result from overinterpreting data extrapolated from one or two patients. It would be several years before the importance of Levy's randomly selected samples would be obvious.
Levy and UCSF colleague John Ziegler had a theory that “AIDS is itself an opportunistic infection. It causes disease only in individuals who are already immuno-compromised by hepatitis B, cytomegalovirus, parasites, or other immunosuppressive factors.”
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They saw the AIDS disease process in fairly complex terms. Probably because their entire patient population in 1983 was composed of gay, sexually active men, they thought AIDS was the final step in a multistaged process that began with an immune system assault by an array of other agentsâparticularly cytomegalovirus and Epstein-Barr virusâafter which an as yet undiscovered “AIDS virus” entered the individual's body.
Levy postulated that “the virus has mutated itself to be such a close imitator of the immune systemâof some component of the immune systemâthat when the system tries to attack the virus, it ends up attacking itself.”
The result, Ziegler said, was a profound autoimmunity, or immune system self-destruction, in which the mighty forces of the B- and T-cell systems mistakenly attacked the body's defenses. Levy's guess was that the observed T-cell imbalances in AIDS patients were the direct result of such a process.
But other scientists were looking at the same data on AIDS patients and reaching very different conclusions. Some felt AIDS was simply a new manifestation of the hepatitis B virus,
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or of some unknown contaminant of the hepatitis vaccine, first experimental trials of which had been on gay Americans.
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or of some unknown contaminant of the hepatitis vaccine, first experimental trials of which had been on gay Americans.
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A variety of other AIDS causality theories floated about the popular and scientific literatures during the early 1980s. Most shared a fundamental flaw: they sought to explain the existence of the disease solely on the basis of observations in the American gay community, ignoring contradictory epidemiological evidence arising from a broader look at all the people who were contracting AIDS. The majority of suggestions put forward by credible scientists were subjected to scrutiny at the laboratory or epidemiologic
level, and then withdrawn or amended by the initial proponents when found lacking.
level, and then withdrawn or amended by the initial proponents when found lacking.
But, as had been the case with so many previous epidemics, there were zealots who denounced their critics in conspiratorial terms and insisted, long after data proved them wrong, that the AIDS causality they had identified was correct. In some cases, their public pronouncements had harsh impacts on the behavior of people who were potentially at risk for AIDS.
Among the early AIDS theories that gained the greatest attention were the notion that the disease was syphilis or that syphilis acted as a co-factor to some other microbe.
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Many physicians continued to insist, despite contrary data, that unique fast-lane practices in the gay communities, including “poppers,” “fisting,” and the use of steroid skin creams, were key.
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A New Zealand team asserted that AIDS was caused by the same tiny odd protein elements then thought to spark scrapie disease in sheep.
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Many physicians continued to insist, despite contrary data, that unique fast-lane practices in the gay communities, including “poppers,” “fisting,” and the use of steroid skin creams, were key.
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A New Zealand team asserted that AIDS was caused by the same tiny odd protein elements then thought to spark scrapie disease in sheep.
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Two American scientists became controversial in 1983âand continued to be celebrated into the 1990s in the
New York Native
âfor their theory that AIDS was caused by African swine fever.
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A serious veterinary problem, ASFV infected a variety of different types of pig cells. Human infections with ASFV were rare events, but could produce fevers and immune system disruptions. The researchers who hypothesized the ASFV/AIDS link noted the intersection of events they believed conspired to create an aberrant form of the microbe: a 1978 outbreak among pigs in Cuba and Haiti, which, they argued, was part of a CIA effort to destabilize the Castro government by destroying its livestock; mass movement of refugees from both islands to the United States in 1980; and alleged consumption of undercooked pork by New York homosexuals while on vacation in Haiti.
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New York Native
âfor their theory that AIDS was caused by African swine fever.
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A serious veterinary problem, ASFV infected a variety of different types of pig cells. Human infections with ASFV were rare events, but could produce fevers and immune system disruptions. The researchers who hypothesized the ASFV/AIDS link noted the intersection of events they believed conspired to create an aberrant form of the microbe: a 1978 outbreak among pigs in Cuba and Haiti, which, they argued, was part of a CIA effort to destabilize the Castro government by destroying its livestock; mass movement of refugees from both islands to the United States in 1980; and alleged consumption of undercooked pork by New York homosexuals while on vacation in Haiti.
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Still others favored the notion that AIDS was caused by “factors” of some kind in blood products used by people with hemophilia.
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Conversely, some argued that all the cases allegedly associated with the blood supply were merely misunderstood ailments of other kinds.
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Thus ignoring evidence that blood product recipients throughout the industrialized world were contracting AIDS and that, when they could be traced, the donors were usually found to have AIDS.
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Conversely, some argued that all the cases allegedly associated with the blood supply were merely misunderstood ailments of other kinds.
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Thus ignoring evidence that blood product recipients throughout the industrialized world were contracting AIDS and that, when they could be traced, the donors were usually found to have AIDS.
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A 1983 Tulane University study of men with hemophilia and their wives proved three key points germane to the causality debate: (1) AIDS in people with hemophilia was precisely the same disease as AIDS in gay men; (2) but the hemophilic patients had no histories of any causes of AIDS proposed for gay men; and (3) some of the men seemed to have passed the disease on to their wives. The researchers concluded that “chronic infection with a blood product-transmissible agent is the most likely source of the abnormalities noted. As hemophiliac patients are not generally exposed to other risk factors previously implicated, future studies ⦠as to the cause” of AIDS ought not to focus solely on “persons with nontraditional lifestyles.”
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The CDC gave out mixed messages in 1983. Concluding their first limited
case control study of fifty gay men with AIDS, the agency researchers said that they “cannot exclude the possibility that ⦠illicit drug use” and “certain aspects of their lifestyle” were correlated with AIDS. Though the CDC team never described lifestyle issues as
causative
, many members of the gay community read the results as supporting a role for “poppers” and such.
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case control study of fifty gay men with AIDS, the agency researchers said that they “cannot exclude the possibility that ⦠illicit drug use” and “certain aspects of their lifestyle” were correlated with AIDS. Though the CDC team never described lifestyle issues as
causative
, many members of the gay community read the results as supporting a role for “poppers” and such.
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Meanwhile, Francis and Dr. Martha Rogers issued word from the CDC lab that beyond higher-than-average levels of CMV and Epstein-Barr viruses, the gay men with AIDS had nothing in their bodies that could explain their terminal illnesses. “We suggest that future laboratory studies be designed to identify an infectious agent that may circulate freely in the blood or with peripheral blood leukocytes, and that may also be found in rectal secretions, semen, or other secretions of homosexual men.”
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Amid the confusion, physicist John Maddox, editor of England's most distinguished scientific journal,
Nature
, penned an April editorial entitled “No Need for Panic About AIDS.”
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Nature
, penned an April editorial entitled “No Need for Panic About AIDS.”
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“There is now a serious danger that alarm about the disease physicians call acquired immune deficiency syndrome (unhelpful, AIDS for short) will get out of hand,” he wrote. “For the characteristics of this previously unrecognized and
perhaps non-existent
[emphasis added] condition are so alarming that the temptation to portray it as a disease invited by a decadent civilizationâa kind of latter-day version of the fate of Sodom and Gomorrahâis almost irresistible.” Maddox denounced the “pathetic promiscuity of homosexuals,” calling it “the most obvious threat to public health.”
perhaps non-existent
[emphasis added] condition are so alarming that the temptation to portray it as a disease invited by a decadent civilizationâa kind of latter-day version of the fate of Sodom and Gomorrahâis almost irresistible.” Maddox denounced the “pathetic promiscuity of homosexuals,” calling it “the most obvious threat to public health.”
Dismissing AIDS as a disease that had occurred among fewer than one thousand people, 70 percent of whom were homosexuals, Maddox berated alarmists, adding that “mercifully, the diseaseâwhatever its causationâis neither especially infectious ⦠nor certain in its effects.”
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