THE EPIDEMIC [ A GLOBAL HISTORY OF AIDS ] JONATHAN ENGEL FOR MY CHILDREN: EZRA, RUTH, MIRIAM, AND JUDAH CONTENTS Prologue 1 1. First Reports 5 2. Growing Panic 25 3. Race to the Vector 55 4. Conservative Backlash 69 5. Organizing and Selling 103 6. Drugs 127 7. The Shooting Galleries 147 8. Who Pays? 175 9. Myths 193 10. Africa 211 11. Breakthrough 233 12. Asia 255 13. Backsliding 267 14. Pandemic 291 Epilogue 321 Abbreviations 327 Notes 330 Acknowledgments 392 Index 393 Other Books by Jonathan Engel Cover Copyright About the Publisher PROLOGUE Sometime in the 1930s, most probably 1931, a small bit of ribonucleic acid (RNA), one of two types of genetic material found in the world, spontaneously mutated.1 This bit of RNA was the carrier of all genetic information for an insignificant virus now known as simian immunode- ficiency virus, which had lived in the bodies of various types of African monkeys and apes for several hundred thousand years. The virus lived parasitically in the apes, hindering them modestly without killing them, and thus enabled its hosts to live and incubate more viruses, generation after generation. The mutation that occurred in 1931 was hardly unique. Genetic ma- terialÐboth DNA and RNAÐmutates frequently, and such mutations are the basic engine of evolutionary change. This particular mutation, however, would prove to be extraordinarily consequential for the world, as it allowed the virus, which could previously live only in its ape hosts, to live in human beings. Once the mutation occurred, random chance dictated that the virus would eventually find a human host. Whether by an African hunter eating an infected monkey, or a chance contamination of an open human sore with monkey blood, the virus would come to roost in a human host, and from there spread to any other humans with whom the primary host shared any of his or her bodily fluids that could harbor the pathogen.2 Such transmission from monkey to human probably occurred multiple times over the ensuing four decades, but for reasons specific to this particular virus, the range of contamination remained limited.3 For one, the virus was unusually weak, unable to survive in air, and often unable to penetrate the skin, epithelial tissue, and the mucosal linings of its host's sexual partners. For another, lack of good roads or commercial air routes into infected areas of Africa prevented the virus from spreading beyond small, isolated tribal groups. And third, the absence of hypodermic syringes in these areas prevented its spread through contaminated needle pricks.4 The virus did spread sporadically, however. At least 19 times between 1950 and 1972 it managed to travel by car, boat, or plane, to infect an isolated individual in a far part of the globe. In 1959, for example, David Carr was admitted to the Manchester (England) Royal Infirmary with a variety of inexplicable symptoms including inflamed nostrils and gums, skin lesions, and severe fever and weight loss. Moreover, his immune system seemed to have wholly ceased functioning. And upon his death, 20 weeks later, an autopsy revealed that he had suffered from a rare form of pneumonia, Pneumocystis carinii (PCP), which was associated almost exclusively with elderly men of Mediterranean or Ashkenazic Jewish extraction.5 That same year, a Bantu man died in Leopoldville, Belgian Congo, after having suffered similar symptoms.6 Other cases retroactively identified in those early years include that of Robert R., a Saint Louis teenager who died mysteriously in 1969 after having been found to suffer from odd swelling of the legs, torso, and genitalia, and whose autopsied body proved to be riddled with a rare skin cancer known as Kaposi's sarcoma (KS);7 a Danish surgeon in 1977 who several years previously had been working in a rural surgical ward in Zaire;8 and a Canadian woman who had once been a nun who left her order in 1972 to rehabilitate prostitutes in Port-au-Prince, Haiti, and who died in Canada in 1981.9 Toward the late 1970s, these early cases, all identified as resultant of similar pathogenic infections, began to appear more frequently. Between 1973 and 1979 at least 5 New York men contracted the myste- 2 / THE EPIDEMIC rious illness,10 as did at least a dozen others in Western Europe, the United States, and Israel.11 But it was from Africa, particularly central Africa, that the preponderance of early cases emanated. Although medical records are scarce for many of the rural populations of that part of Africa, retrospective tests on collected sera conducted one to two decades later showed presence of the mysterious virus in the blood of decedents in Zaire from the early to mid 1970s, in over 50 cases.12 By 1982, Zaire, alone, had produced 18 identifiable victims of the strange new disease, all of whom had sought care in Belgium.13 Years later, after the mutated pathogen had been identified, mapped, charted, described, explored, and blamed for the death of tens of millions of people, scientists would debate how and when the bit of RNA had jumped species. Was it definitely in Africa, or was this merely another example of a Eurocentric establishment blaming their ills on the dark continent? And if it had been in Africa, could the cause have been rooted in human actions? One tenacious author seized on the explanation that the virus, or at least one iteration of it, while of monkey origins, had actually been inadvertently included in batches of oral polio vaccine that were administered to patients in the Belgian Congo in the late 1950s.14 The thesis, while compelling, and perhaps even titillating, couldn't stand up to rigorous investigation. As cases became known that predated the vaccine administration, and as genetic researchers confidently dated the primary mutation to two decades prior, the thesis was dismissed.15 The truth, it turned out, was more mundane. The troublesome pathogen was one of several that had mutated more toxic qualities during the course of the 20th century, and lodged in human hosts. Others, such as Ebola and Marburg, had arisen as rapidly and mysteri- ously. This one, however, had spontaneously stumbled upon the sublime trick of slow pathogenesis. While other fatal viruses killed so rapidly that they scarcely gave their hosts time enough to transmit the virus before dying, this one killed slowly. In the decade or so that it took the virus to wholly immobilize its host's immune system, and ultimately kill him, the host could spread the virus to hundreds of unknowing new hosts, whether through sexual coupling, needle sharing, or blood transfusions. And for much of that decade, the symptoms of the viral infection were so mild that the pathogen's presence remained all but unknow- JONATHAN ENGEL / 3 able. The one great defense on the side of the humansÐthe essential weakness of the virus's protein coatÐprotected humans for decades. Once the virus breached the jungle, however, and learned to travel by automobile and jet, that defense was no longer adequate. Our story starts, then, not at the inception of the new virus, but at the moment it entered the modern world. For it was here that the virus found fertile ground to grow and spread, jumping intercontinentally in a matter of months, and growing exponentially in frequency, until it overwhelmed whole communities, towns, cities, and even nations. Our story starts in the raucous Castro and Greenwich Village neighbor- hoods of San Francisco and New York City in the early 1980s, where a weird amalgam of unprecedented eroticism and fierce political defiance combined to create a near perfect environ for the virus's spread. 4 / THE EPIDEMIC CHAPTER 1 FIRST REPORTS FIRST REPORTS In June of 1981, the United States Centers for Disease Control (CDC) reported that five young men in Los Angeles had been treated in recent months for Pneumocystis carinii (PCP), a rare form of pneumonia. Two had later died. All were also infected with, or had been infected with, cytomegalovirus (CMV).1 All were active homosexuals. All had had multiple sexual partners over the past several years. Several had repor- ted using one of two sexual enhancement drugs: LSD or amyl nitrite.2 Two months later, the CDC reported that over 100 gay men had been diagnosed with either PCP or a rare cancer, Kaposi's sarcoma (KS), since January of 1980. Nearly half had died. Some men had been dia- gnosed with both maladies, others with only one. Typically, the CDC reported, KS afflicted only 1 American in 1.5 million, and the victims were predominantly elderly.3 The cause was unclear. Harold Jaffe, a member of the CDC group investigating the malady, queried whether this new syndrome affected only gay men, or if gay men were simply being disproportionately diagnosed. The CDC began to track the syndrome that fall, using re- quests for pentamidine isothionate, a drug used to treat PCP, as a means of locating the cases. Many of the diagnosed men had contracted other sexually transmitted diseases, or had been diagnosed as well with various sorts of mucosal infections and digestive parasites. The one significant factor in the cases appeared to be the number of sexual partners with which the infected men had liaised over the previous year: over 60 for the infected men versus 25 for a control group.4 Most troubling was the rate at which the peculiar syndrome appeared to be spreading. Case frequency seemed to grow exponentially. ªIf I had written this a month ago, I would have used the figure `40,'º wrote gay playwright and activist Larry Kramer that September.