The Coming Plague

by Laurie Garrett

  “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 1983.70 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.71 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.”72

  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 agents—particularly cytomegalovirus and Epstein-Barr virus—after 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 system—of some component of the immune system—that 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,73 or of some unknown contaminant of the hepatitis vaccine, first experimental trials of which had been on gay Americans.74

  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.

  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.75 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.76 A New Zealand team asserted that AIDS was caused by the same tiny odd protein elements then thought to spark scrapie disease in sheep.77

  Two American scientists became controversial in 1983—and continued to be celebrated into the 1990s in the New York Native—for their theory that AIDS was caused by African swine fever.78 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.79

  Still others favored the notion that AIDS was caused by “factors” of some kind in blood products used by people with hemophilia.80 Conversely, some argued that all the cases allegedly associated with the blood supply were merely misunderstood ailments of other kinds.81 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.82

  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.”83

  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.84

  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.”85

  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.”86

  “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 civilization—a kind of latter-day version of the fate of Sodom and Gomorrah—is 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 al
armists, adding that “mercifully, the disease—whatever its causation—is neither especially infectious … nor certain in its effects.”

  By contrast, during the spring of 1983, Curran, Francis, and Harvard’s Max Essex collaborated on an editorial wake-up call to be published in the Journal of the National Cancer Institute. Their intention was to state in no uncertain terms that AIDS was caused by an infectious agent and to suggest that one of the candidates for causation of AIDS was HTLV-I.87 Essex already had evidence that many AIDS patients were infected with HTLV-I.

  “We checked a series of 75 patients with AIDS that were sent to us from CDC,” Essex explained in May. “And the patients were classified as either having Kaposi’s or Pneumocystis. And in that series of 75 … between a quarter and a third of the patients had evidence of prior exposure to the HTLV.

  “One possibility that I should underline is that the HTLV has nothing to do with this disease, and that the HTLV is opportunistically infecting some of the patients with AIDS, but not all of them,” Essex hastily added.

  Gallo was ecstatic. Essex had evidence that implicated his personal nominee for the AIDS culprit. Gallo’s lab staff had just isolated HTLV-I from the white blood cells of three New York City gay men with AIDS, and in a survey of 33 AIDS patients in New York Hospital, Gallo’s group found HTLV-I in the T cells of two men. Together, these findings seemed to argue strongly, in Gallo’s view, that HTLV-I, or one of its close cousins, caused AIDS.

  The four Essex and Gallo papers were published as a package in the journal Science, along with a study from the Pasteur Institute group that an official U.S. Department of Health and Human Services press release that day described as reporting “isolation of an HTLV-related virus from a homosexual patient with persistent, multiple lymphadenopathies and evidence of infections who may be at risk of developing AIDS.”88

  But that wasn’t what the French study showed. Not at all.

  On February 4, 1983, the Pasteur Institute’s Charles Dauguet observed dozens of spherical viruses poking out of Frederic Brugière’s T cells. However, though the mysterious viruses under Dauguet’s microscope and HTLV-I were both spherical, they did not appear to the French scientist to he identical. More importantly, Montagnier’s group was unable to get strong cross-reactivity between antibodies against Gallo’s HTLV-I virus and their AIDS-related microbe. They suggested that the two agents might share some genetic similarities, but were clearly different species of viruses.

  Nevertheless, at Gallo’s urging Montagnier had inserted the following in his article: “We tentatively conclude that this virus, as well as all previous HTLV isolates, belong to a family of T-lymphotropic retroviruses that are horizontally transmitted in humans and may be involved in several pathological syndromes, including AIDS.”

  Throughout the summer of 1983 the two competing laboratories toiled to grow the apparent AIDS viruses in cell cultures. But the viruses only grew well inside human T cells, which they also killed. So in a matter of days all the cells in a culture would be dead, along with the elusive viruses. Barré-Sinoussi and Chermann tried a variety of unsuccessful strategies to grow the viruses. Finally, during the dog days of summer Montagnier’s team figured out that the trick was continuously, every three days, passing virally infected liquid (supernatant) from cells grown in the presence of T-cell stimulators interleukin-2 and phytohaemagglutinin to fresh T cells, and repeating the process over and over for several weeks. Eventually one would get a culture dish chock-full of viruses.

  Meanwhile, panic was growing in North America.

  Though the absolute number of reported AIDS cases in Canada and the United States was still below 2,000, the dimensions of the epidemic were expanding. Drs. James Oleske at the New Jersey Medical School in Newark and Arye Rubinstein of the Albert Einstein School of Medicine in the Bronx were treating babies and toddlers who seemed to have contracted AIDS from their parents. Oleske was treating eleven such children, Rubinstein twenty-five.89 All of the children had a parent who either used injectable narcotics, had recently emigrated from Haiti or the Dominican Republic, or was “promiscuous,” as the physicians put it.

  “Clearly none of the children that we have seen were sexually abused or given illicit drugs,” Oleske said in May 1983. “So the implications are that, if you will, ‘normal’ people can acquire AIDS.”

  Rubinstein agreed, saying that it was likely most of the children got the presumed AIDS virus from their mothers during or immediately after pregnancy, but “we find discrete immune deficiencies in other members of the [families his group was studying]. Something that may suggest that the transmissible agent can be acquired in a different mode: not only transplacentally, not only sexually, not only by sharing of needles.”

  In early 1983, a joint CDC/Montefiore Medical Center study in New York City described two women with AIDS who had no other apparent risk factors save marriage to men who had the disease.90 By May, Montefiore’s Dr. Neil Steigbigel had uncovered five more cases of apparent heterosexual transmission.

  “We do feel now that this does show that AIDS should be considered threatening to the health of our general population, not only to male homosexuals, abusers of intravenous drugs, Haitians, or hemophiliacs,” Steigbigel said at the time. “Of course, if one is dealing with a potentially fatal disease, that is tremendously frightening. To have a potentially fatal venereal disease, that is … present in our general population.”

  Other studies confirming the sexual passage of the mysterious AIDS agent flooded in during the summer and fall of 1983.

  In many ways the most alarming news for the CDC’s AIDS Task Force members came from the users of injectable drugs. Curran, Jaffe, Francis, Guinan, Darrow, and the others all cut their public health teeth on sexually transmitted diseases; even so, they were surprised, even shocked, by what they learned about the sexual fast lane in the gay community. Before AIDS, they were similarly ignorant about the drug-using population. They didn’t know about all the years that Greggory Howard, and thousands like him, had been stashing their “works” in shared hiding places. They didn’t know about the allegedly abandoned buildings filled with the commerce of narcotics.

  When New York City and Newark drug researchers brought their familiarity with the desperate details of drug addiction into the growing circle of American AIDS scientists, their insights hit Curran and his colleagues with a jolt: one could debate theoretical probabilities of contracting AIDS through sexual transmission, but injecting it into one’s bloodstream seemed to guarantee infection.

  Soon the CDC group was learning about shooting galleries where junkies could pay to get injected with just about anything by a dealer who used the same needle and syringe on dozens—even hundreds—of customers a day. Experts like Dr. Don Des Jarlais, who ran a drug rehabilitation program inside Manhattan’s Beth Israel Hospital, told the CDC scientists that few addicts in 1983 used just one drug: they were addicted to two, three, or more drugs, often including cocaine, alcohol, amphetamines, barbiturates, Valium, and other benzodiazepines. After years of periodic heroin “famines,” due either to police actions or to wholesaler market manipulations, expert narcotics users had adapted by mixing their drugs. One “cocktail” to start the day, another to smooth the rocky edges of coming down off the first, and still another to shoot the user straight to temporary paradise.

  It was naive in the extreme, the CDC scientists learned, to build stereotypes around junkies, or to assume that any single behavior explained the skyrocketing increase in AIDS among users. The array of individual drug-use patterns could range from lethargy to hyperactivity. These people were neither easy to study nor easy to educate.

  “We just don’t know what to make of all of this,” Curran said. “We can’t explain w
hy almost all IVDU (intravenous drug user) cases are showing up in New York and New Jersey, while most of the West Coast cases—more than 90 percent—are among gay men. We don’t really understand the distribution.”

  “All you have to do is walk the streets,” Howard would claim. “Greggory knows what’s going on.”

  Howard was trying to stick with methadone, but it was tough. The clinic staff treated the junkies like animals, he said, and it was often questionable which was more demeaning: pulling down your pants in front of a hulking clinic guard and struggling to pee into a Dixie Cup while in drug withdrawal so they could test for heroin; or searching frantically for a usable vein to bare to a scowling dealer who jabbed the needle in, shoved down the plunger, released the tourniquet, and turned to the next customer while you swayed off into suspended animation.

  Though Howard didn’t yet know much about AIDS by the fall of 1983, he was an expert on lifestyles of the stoned and addicted. He could have told the CDC team enlightening and unsettling stories, if they had bothered to ask. But they didn’t. Curran knew his team was out of their depth when it came to injecting drug users, and he lobbied hard for research efforts at the agencies that were supposed to be on top of such things, particularly NIDA (National Institute on Drug Abuse). But under the Reagan administration, NIDA was far more concerned with eliminating drugs than with keeping users alive.

  If anybody had asked him, Howard would have told the government scientists the same things he said to anyone who asked. “How much Greggory uses,” Howard would say, “when he uses it, how he uses it, all depends on what he’s using. It’s as simple as that.”

  If it boiled down to nothing more than heroin—which it rarely did—one or two injections per day with his personal works would be adequate. If, however, he mixed heroin with downers like alcohol or barbiturates, and “wildness” like injected cocaine or speed, things got more complicated. 91 Heroin might last for hours, but cocaine’s rush persisted for only minutes. A heavy injected dose of speed might have the user walking through Newark, barefoot and unfueled by food or sleep, for two or three days unless he smoothed it over with some serious downers, like Valium or barbiturates, both of which would come on faster if the pills were washed down with high-proof alcohol.