The Pandemic Century

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“This is a very, very dramatic illness. I think we can say,

  quite assuredly, that it is new.”

  —JAMES CURRAN, epidemiologist, 1982

  In December 1980, Dr. Michael Gottlieb was looking for an unusual teaching case to present to residents at the University of California Medical Center Los Angeles (UCLA) when one of his colleagues stumbled on a patient named Michael. A thirty-three-year-old artist, Michael had been admitted to the emergency room suffering from extreme weight loss and looked like an anorexic. In addition, his mouth was full of thrush, or candidiasis, a yeast infection usually seen in patients with weakened immune systems. Intrigued, Gottlieb, then a young assistant professor specializing in immunology, led residents to Michael’s bedside and afterwards discussed the case with them. “There was something medically interesting about him,” Gottlieb recalled. “He smelled like an immune deficiency.”

  Gottlieb’s intuition was correct: Michael’s antibody-producing capacity seemed to be intact, but when a colleague ran a specialized test using the latest monoclonal antibody technology he discovered that Michael had very few T cells. In particular, he found that a subset of Michael’s T cells, known as CD4 cells, were perilously low. The central controllers of the immune system, CD4 cells are required for every type of immune response—whether to signal CD8 “killer” cells, whose job it is to destroy virus-infected cells; activate macrophages, a type of white blood cell that patrols for pathogens; or alert B lymphocytes, which produce antibodies against foreign invaders. Once these CD4 cells have been eliminated, sooner or later the entire immune system crashes. Their absence almost certainly explained the thrush. According to Gottlieb, the yeast infection was so extensive that Michael’s mouth looked as if it was full of “cottage cheese.” But it was impossible to arrive at a definitive diagnosis, so Michael was discharged. However, within a week he had developed pneumonia and had to be readmitted.

  Concerned that Michael might have contracted an opportunistic lung infection, Gottlieb convinced a pulmonary specialist to perform a bronchoscopy and send a sample of his lung tissue to the laboratory. To Gottlieb’s surprise, the tissue came back positive for Pneumocystis carinii pneumonia, or PCP, a rare fungal infection seen almost exclusively in malnourished newborns and infants in intensive care, terminally ill cancer patients, or the recipients of organ transplants. What such patients shared in common was compromised immune systems. For a young man to develop PCP was practically unheard of. “It was a distinctly unusual thing for someone previously healthy to walk into a hospital so significantly ill. It just didn’t fit any recognized disease or syndrome that we were aware of.” By March, Michael had been hospitalized, but no amount of drugs or experimental therapies would arrest the progress of the infection, and in May 1981 he died. The autopsy found pneumocystis throughout his lungs. Later, trying to figure out what could have caused Michael’s immune system to give up on him, Gottlieb reviewed the artist’s medical charts and saw that he had a cornucopia of sexually transmitted diseases (STDs). He also recalled a conversation in which Michael had mentioned that he was gay, but then Los Angeles had long boasted a sizable gay community, so it was difficult to see what bearing this could have on the matter.

  Gottlieb was not the only doctor in Los Angeles to spot an unusual constellation of symptoms in gay men that fall and winter. The previous October, Joel Weisman, a local physician with a largely gay practice, had also treated two men for thrush. In addition, the men had chronic fevers and suffered from diarrhea and lymphadenopathy—swollen lymph nodes. In February one of the men’s symptoms worsened and he was admitted to UCLA, where Gottlieb tested his blood and found the same abnormality that Michael had: a lower than expected number of CD4 cells. Soon after, he also developed PCP, as did the second patient in Weisman’s care. In addition, both men had active cytomegalovirus (CMV), a type of herpes virus which is spread in bodily fluids, typically through kissing and sex, and which is usually quiescent in healthy adults. By April Gottlieb was becoming sufficiently concerned to call a former student, Wayne Shandera, now a member of the CDC’s Epidemic Intelligence Service in Los Angeles. Gottlieb told Shandera of his suspicion that there was a new disease circulating in Los Angeles and asked him to check the LA County health records for other reports of PCP and/or CMV. Shandera quickly located a report about a man in Santa Monica who had recently been diagnosed with Pneumocystis and was deathly ill in the hospital. Soon after Shandera’s visit, the man died and, on autopsy, CMV was found in his lungs.

  Unbeknownst to Gottlieb and Weisman, by now physicians in New York were also seeing similar cases of swollen lymph nodes, low CD4 cell counts, and PCP in gay men in their care. At autopsy many were also found to be infected with CMV. Observing these patients up close was a shocking experience. Donna Mildvan, chief of infectious disease at Beth Israel Hospital, New York, recorded how in one case involving a German man who had formerly worked as a chef in Haiti and who had died in December, she had cultured CMV directly from his eyeball. “We were totally bewildered. . . . I can’t even begin to tell you what an awful experience it was.” Dr. Alvin Friedman-Kien, a dermatologist and virologist at New York University’s Medical Center, was similarly disturbed to find that many of the patients also had Kaposi’s sarcoma (KS), an extremely rare type of skin cancer typically seen in elderly Jewish men or men of eastern European and Mediterranean descent. Most dermatologists might go their whole career and see only one case of KS, but by February Friedman-Kien was aware of twenty cases of KS in the New York area alone. One of the most heartbreaking involved a young Shakespearian actor who presented at Friedman-Kien’s practice in January with pink-purple spots on his face. The spots were so extensive, Friedman-Kien recalled, “he couldn’t cover them up anymore.”

  In medicine, as in other professions, being first is everything—no one remembers the second person to describe a new disease—and by June Gottlieb was ready to go into print, informing the editor of the New England Journal of Medicine that he had “possibly a bigger story than Legionnaires’ Disease.” By now Gottlieb had five severe pneumonia cases (the fifth had come to him via a Beverley Hills physician). All were gay men between the ages of twenty-nine and thirty-six, all had PCP, candidiasis, and CMV, and three had low CD4 cell counts (in the two others, immune deficiency had not been studied). In addition, Gottlieb and Weisman noted, all five had also used “poppers”—amyl nitrate or butyl nitrate inhalers so named for the noise the ampules make when broken. However, their leading hypothesis at this stage was that the disease was due to CMV and, perhaps, some other virus, such as Epstein-Barr, interacting with one another so as to compromise the immune system. From a public health point of view this was worrying. Sexual health clinics across the United States had recently seen a marked increase in CMV cases which, along with other sexually transmitted diseases, such as hepatitis B and gonorrhea, were running at epidemic levels in the gay community.

  Given the interest in getting the announcement out quickly, the editor of the New England Journal of Medicine advised Gottlieb to submit a brief article to the CDC’s Sexually Transmitted Diseases division for publication in the agency’s house journal, Morbidity and Mortality Weekly Report, on the understanding that the New England Journal of Medicine would consider a longer article at a later date. Jim Curran, the official who headed the STD division, immediately recognized the article’s significance, not least because he was concerned about the recent increase in STDs in gay men and had been working closely with the homosexual community to evaluate the risk factors for hepatitis B. Before publishing the article, however, he asked a female colleague to check whether there had been any other reports of PCP in people without cancer, or who had not received organ transplants and had been taking drugs to suppress their immune systems. Looking back over fifteen years, she could find only one such case. Alarmingly, however, orders for pentamidine, an anti-PCP drug that was no longer in commercial production and for which the CDC had a small emergency stock, had jumped from the usual fifteen request
s a year to thirty in the first five months of 1981. Curran did not require further convincing, and on June 5, 1981, he published Gottlieb’s article in the Morbidity and Mortality Weekly Report together with an accompanying editorial. Noting that PCP was almost exclusively limited to severely immunosuppressed patients, Curran commented that its occurrence in previously healthy individuals was “unsettling,” and the fact that all five individuals were gay suggested “an association between some aspect of a homosexual lifestyle or disease acquired through sexual contact and Pneumocystis pneumonia in this population.” Although no definite conclusion could be reached about the role of CMV infections, Curran also noted recent surveys showing that many homosexual men carried CMV in their semen and that “seminal fluid may be an important vehicle of CMV transmission.” In other words, there was no evidence that CMV was the cause of the mysterious new syndrome, but sexual transmission was suspected. Though hedged with qualifications, Curran’s conclusion was prophetic: “All the above observations suggest the possibility of a cellular-immune dysfunction related to a common exposure that predisposes individuals to opportunistic infections such as pneumocystis and candidiasis.” No one could have imagined that within months of that article appearing, these strange symptoms would be the talk of Hollywood, and by the following summer the world would have learned a terrifying new acronym. Curran may not have realized it but he had just described AIDS, acquired immunodeficiency syndrome.

  IN THE FORTY YEARS SINCE—the CDC settled on the acronym in 1982—public attitudes toward AIDS have gone from indifference, to horror and dread, to seeing it as just another infectious disease, one that can be treated with an arsenal of drugs that suppress but never quite eliminate the human immunodeficiency virus (HIV), which is the cause of the immune deficiency that allows the opportunistic infections with which AIDS is associated to occur. In this transition from fear to familiarity, it is easy to forget the shocking sight of the first AIDS patients and the dismay they provoked in doctors powerless to help them. As David Ho, a physician at the Cedars-Sinai Medical Center, recalled, those early patients “looked like concentration camp survivors.” Adding to the dismay was the fact that the causes were “completely unknown.” As the true extent of the epidemic became evident—in 1982 the number of AIDS cases in the United States totaled 593; two years later there were nearly 7,000 cases and there had been over 4,000 deaths—AIDS came to be regarded as a plague (the “gay plague” to be specific) and the signal of a disastrous return to a former historical epoch when the plague and other epidemic diseases had routinely ravaged human communities. If Legionnaires’ disease had been a warning to an overly complacent public health profession, then AIDS was the epidemic that drove home the lesson: despite vaccines, antibiotics, and other medical technologies, infectious disease had not been banished but posed a continuing and present threat to technologically advanced societies. Worse, as scientists learned more about the disease and its origins, it soon became apparent that sex and medical technologies—in particular, the wide provision of hypodermic needles and reusable syringes via public health programs and other humanitarian medical initiatives in Africa, plus blood banks and blood transfusion services—had greatly amplified transmission of the virus, transforming what had been scattered, isolated cases in Africa into a widely dispersed infection which eventually became a pandemic. Even so, no one could have imagined that by the end of the twentieth century 14 million people would have died of AIDS globally and 33 million more would be living with the virus. Or that by 2015, a further 36 million people around the world would have contracted HIV, and some 40 million would be dead, a figure that approaches the mortality of the Spanish flu.

  As we shall see, the AIDS pandemic was not only the result of technological interventions; as with psittacosis, economic, social, and cultural factors also likely played a part. In particular, the emergence of AIDS appears to have been connected to the construction in the colonial period of new railways and roads in equatorial regions of Central Africa, projects that fueled the influx of male laborers into rural areas, destabilizing gender relations and fostering a culture of prostitution in Léopoldville (Kinshasa) and other large towns and cities. The loosening of sexual taboos following gay liberation was a similarly important factor in the spread of AIDS in the United States, particularly in cities like New York and San Francisco where bathhouses became venues for unprotected anal sex between men boasting multiple sexual partners. However, it would appear that such practices only contributed to the explosion of AIDS in America after HIV had been imported to the United States from Haiti in the late 1960s.

  In many respects, AIDS is the exception to the epidemics and pandemics canvassed in this book. Unlike influenza or Legionnaires’ disease, medical researchers could hardly be accused of being blinded by overconfidence in 1981. Nor could the CDC be accused of being complacent about the threat posed by sexually transmitted diseases in the early 1980s, or of failing to recognize AIDS’s peculiar constellation of symptoms sooner. On the contrary, AIDS might have continued its slow, stealth-like spread for several more years had it not been for key conceptual advances in oncology and new laboratory technologies that, for the first time, gave clinicians the possibility of identifying the depletion of CD4 cells that is the signature of advanced HIV infection, and medical researchers the ability to continuously grow T cells in culture. Indeed, reflecting on the history of AIDS, Robert Gallo, the NIH cancer specialist who would share credit for the discovery of HIV with Luc Montagnier of the Pasteur Institute, argued that had AIDS struck in 1955, scientists would have been “in a dark box,” so limited was the contemporary understanding of retroviruses and scientists’ ability to study them. “No one would have believed in this kind of virus. They did not even know what this kind of virus was,” he told an interviewer in 1994. Even in the 1960s and early 1970s, he argued, scientists would have struggled to comprehend HIV. Or, to put it another way, the AIDS epidemic broke out at precisely the moment when, for the first time in history, scientists working in oncology and the specialized area of human retrovirology were inclined to believe that a retrovirus might be the cause of the peculiar new syndrome and possessed the tools and technology to test the hypothesis. Even so, from the beginning of the hunt for the virus of AIDS, research was clouded by presumptions about what sort of retrovirus HIV would turn out to be, and nowhere more so than in the mind of Gallo.

  TODAY, IN AN ERA of antiretroviral drugs, when a diagnosis of AIDS is no longer an automatic death sentence, it is easy to forget the panic, hysteria, and stigma of the early days of the pandemic. For conservative politicians such as Jesse Helms, the former Republican senator from North Carolina, and Moral Majority leader Jerry Falwell, AIDS was nothing less than “God’s judgment” and divine retribution for homosexuals’ “perverted” lifestyles. Others argued that the virus had something to do with voodoo; hence, the way it appeared to target Haitians. Still others thought it had been transported to Earth on the tail of a comet from outer space, or that the virus had been incubated in a bioweapons lab by the CIA with the connivance of the Pentagon and Big Pharma.

  In fact, HIV is a special type of virus called a retrovirus. Due to its long latency and gradual onset, it is also classed as a lentivirus (from the Latin term for slow). When a person is first infected with HIV, the immune system produces antibodies to fight off the virus. This process of acute infection can take anywhere from two weeks to three months. During this period, virus levels in the blood are very high and patients are extremely infectious. Victims may also experience flu-like symptoms such as fever, rash, muscle aches, and joint pains, but frequently the symptoms are so mild they pass unnoticed. After seroconversion, HIV usually betrays no further outward sign of its presence for several years. Instead, it works by stealth, silently parasitizing CD4 cells and colonizing the lymphatic system. During the silent phase of infection, HIV uses the machinery of CD4 cells to make copies of itself and spread throughout the body. At each stage, CD4 cells are repeatedly activ
ated and die off. This cycle of activation followed by cell death continues until the body’s capacity for replenishing CD4 cells is exhausted, a process that takes around ten years, but can be shorter or longer. Eventually, without an adequate supply of CD4 cells, the immune system can no longer signal B cells to produce antibodies, or CD8 cells—also known as T cells—to kill infected cells. It is at this point that a victim becomes susceptible to opportunistic infections and develops prominent signs of illness. Until then, however, HIV is quiescent: it lies hidden from view inside CD4 and other immune cells.

  Measuring CD4 cells is the most important laboratory indicator of a person’s immune status and how well their immune system is coping with the virus. Viral load shows the amount of virus in the blood and gives an indication of the risk of progression and transmission, but without the ability to count Michael’s CD4 cells, Gottlieb would have had no idea that his immune system was compromised and that he might be the victim of a new condition. In retrospect, it is astonishing to think that this technology became available at precisely the moment when AIDS first emerged in Los Angeles and other US cities. That the technology was available at UCLA and other hospital immunology departments could largely be attributed to the work of an Argentine émigré, César Millstein, and a German biologist, Georges Köhler. In 1975, these scientists found a way to produce an immortal cell line capable of producing endless quantities of antibodies that targeted specific antigens. Known as monoclonal antibodies—or Mabs for short—the technology removed the need to laboriously isolate and purify antibodies from laboratory cultures, and was soon being used in everything from the rapid typing of blood and tissue, to the development of new drugs against infectious diseases. Soon, Mabs were also aiding the study of leukemia, and by 1981 commercial Mab technologies also became available to distinguish one population of T cells from another. Thus it was that in the winter of 1981 Gottlieb’s colleague found a virtual absence of CD4 cells in Michael’s blood, suggesting that his symptoms were the result of an immune deficiency.

 

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