by Rose George
Pharmaceutical companies lowered the price of first-line drugs (those that are given initially) for developing countries, but not for second- and third-line. MSF has found resistance to first-line drugs at a rate of 10 percent in southern Africa. A study in Kenya, Malawi, and Mozambique found 30 percent of people on second-line treatment had become resistant. Third-line—what is called “salvage therapy”—costs $1,859 a year.35 That is eighteen times more than the cost of basic first-line treatment, and six times more than second-line, and unaffordable for most developing and even developed nations.
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For Eric Goemaere, there will be no true solution for years. “No pandemic has ever been solved without a vaccine,” he says. That is years away. As long as girls have blessers and older boyfriends, and boyfriends have many girlfriends, and men rape, there will be new infections, and prevention and treatment are like pouring water into a sink with an open drain. “The dream is slowly being shattered,” says Goemaere. He is sure we are approaching a second wave of the epidemic, “made out of resistance and treatment fatigue.” But also donor fatigue. Media fatigue. A lowering of the guard on all fronts. He would like to see injectable ARVs or PrEP implants (you can remove an implant if it goes wrong, but not an injection). He was pleased to see a session on implants in Paris. Meanwhile, he does what he can and is hopeful of dolutegravir, a new and “very robust” ARV that is widely available in Europe but nowhere in South Africa. He has taken to bringing it back with him, in his pockets, as he did in the days of TAC.
People are trying hard on all fronts. Scientists are working on vaginal microbicides for women; on vaccines; on viral vectors, other viruses that can transport defenses against HIV. The virologist Paul Bieniasz thinks there is no lack of ingenuity in the fight to beat HIV. “We’re limited more by our technology rather than our brains in trying to figure out how this stuff works.” In various African countries, cash payments have been made to schoolgirls and young women, in an attempt to undercut the poverty that drives some transactional sex. In some countries payments reduced rates of HIV infections, but in others there was no difference. MSF’s pre-exposure prophylaxis program is young. Only forty young women were enrolled at the time of my visit, but this is still promising. There are serious barriers to be scaled: young women don’t want people to think they have HIV because they have medication that looks like ARVs. They worry about stigma and about being accused of sleeping around. The ones who have signed up are the brave ones. In 2017, the health minister of South Africa launched She Conquers, an initiative to stamp out the practice of blessing and to encourage younger women to stay away from older men. It’s an unlikable name, the kind devised in dull boardrooms by dulled brains, and the literature isn’t much better. But it’s a start.
But what about the men? What about Themba and his at least three women and his whiskey sex? Who will protect the young women of South Africa from men like him? In the 1990s, Uganda launched a highly successful behavior modification program with the slogan Zero Grazing.36 Grazing was having more than one partner. Uganda wanted people to stick to main meals. It worked; condom use increased dramatically and Uganda’s HIV prevalence dropped. Then conservative Christian ideology arrived from the United States along with PEPFAR money and found a receptive home in President Museveni and his wife, and condoms were burned, and HIV came back.
HIV is remarkable. Amazing. Elegant. These are words that microbiologists and virologists use, though they always catch themselves. They are quick to counter these words with others. Pandemic. Devastation. Grief. HIV has brought us all these things. But I understand their wonder at the virus. Despite many millions of dollars and forty years of research and countless remarkable minds working on curing HIV, it is only contained and only for now. What does HIV like best? Presumption and assumption that it is beaten.
On the side of the shopping center opposite the MSF offices, the one with the fish and chips shop that is safe to go to if there are enough people around, there is a mural. It is large and can be seen from a mile away (a fact I can prove, as sat navs, given MSF’s address, unfailingly chose to send drivers somewhere else, and the mural became my guide, my crumbs through the forest). This mural shows a young black woman, her hair not Brazilian or Peruvian but natural; her clothes patterned with African designs. She stands against a yellow sky, and a dark green forest rises on a hill behind her. I look at her, not just to find my way around Khayelitsha but because of her face. She is grimacing, the face of someone blinded by the sun, and her hands are clasped above her eyes to give her shade. She squints into the distance, this young woman who looks strong but who statistics say is still too vulnerable to violence and abuse and infection. I want her to triumph because she deserves to. I know that countless people are working ferociously to find cures, solutions, innovations, outreach, to marshal every weapon against HIV. I know all that and try to remember it. But I also know the numbers. So I see this young black woman looking into the distance, and I see her seeing that HIV is coming. It is still coming despite our best efforts and it is coming for her.
Coupon incentive for students to sell plasma
FIVE
THE YELLOW STUFF
A boy opens a fridge and removes two small bottles. He takes a syringe, clean and new. He sits himself somewhere comfortable, clean and well lit: the kitchen table will do. He wears a woolen tank top because he is being filmed at some point in the early 1980s when woolen tank tops were normal, not retro. He inserts the needle into the bottle and draws up the liquid, and he mixes it with the other bottle, and he injects ten thousand people into his right arm, into the crook of his elbow. He looks at the camera, and he grins with joy.
Let blood sit. After a few hours, gravity will partition it: red blood cells below, then a narrow white layer—the buffy coat—that holds white blood cells and platelets. Above, there will be a liquid the color of straw. This is plasma, a liquid that makes up just over half the volume of blood. It carries fat globules, water, salts, and at least seven hundred proteins such as albumin, antibodies, and clotting factors.1 It looks like nothing much next to the insistent red of the blood below. It’s just yellow stuff. But it is worth a fortune.
Separated from a donation of whole blood, plasma becomes fresh frozen plasma (FFP) and is used in transfusions to bulk up volume in bleeding or trauma patients. This is usually collected by blood banks and called recovered plasma. But plasma can have an alternate future where it is not a human body part but a product. Plasma companies collect it from paid donors using aphaeresis machines, which spin whole blood, retain the plasma, and return the rest to the recipient. This is source plasma, and it is purified for its components such as immunoglobulins, which boost immune deficiencies, or albumin, the most common plasma protein, which can maintain blood volume and pressure. These components have come to be known as plasma protein therapeutics. A unit of FFP is cheap: the NHS sells one for under £30 ($42).2 A fraction of source plasma is not. The most popular, intravenous immunoglobulin (IVIG), often costs more than gold (the NHS buys it for about £35 [$49] a gram),3 and one plasma donation can reap medicines worth ten times what a donor is paid (usually about $30). Human and animal blood is the thirteenth most traded commodity in the world, worth $252 billion. Most of that is products derived from plasma, and most of it is coming from the United States, the largest exporter of plasma. In 2016, the category of “human and animal blood”—actually mostly blood fractions such as plasma products—earned the United States $19 billion, close to what it got from selling medium-size cars or soybeans.4 The chief of America’s Blood Centers, an association of blood banks, has called it the OPEC of plasma.5 Half of Europe’s plasma for medicinal products comes from American veins.6
The small boy is grinning because of what was in the bottle. It was plasma-derived clotting factor. Specifically, it was Factor VIII, the name of both a protein found in normal human plasma and a commercial product developed in the 1980s that was usually shortened to “factor.” He is in Engla
nd but the boy has almost certainly just injected a product derived from American plasma sellers. It has revolutionized the lives of millions of hemophiliacs like him. It would also kill them.
When blood escapes the blood vessels, either inside or outside the body, it performs what is called with scientific poetry a clotting cascade. About twelve things need to happen for blood to clot, that seemingly easy procedure that is triggered when you nick your ankle shaving your leg, or cut your finger with a knife, or pick a scab. That thickening of the blood, quickly done, that seems so easy but is not. If any component of the cascade fails, blood will continue to flow. If the blood continues to flow, you are probably a hemophiliac. If a knock to your knee or elbow or head causes you to bleed internally, without stopping, then you are probably a hemophiliac.
One in five thousand boys is born with hemophilia A, says the US National Hemophilia Foundation. (A is the more common variety and means that blood lacks Factor VIII; there is also hemophilia B, due to a lack of Factor IX. The results are the same: you don’t clot properly.)7 The World Federation of Hemophilia suggests a rate of one in ten thousand.8 Take either figure: hemophiliacs are still rare enough that most people are unlikely to encounter one. A hundred years ago, they would have been rarer because they died young. Hemophiliacs are born with a genetic abnormality inherited from their mothers that prevents blood from clotting. It used to be accepted that women only carried and passed on the faulty gene responsible. But now we know that women can be bleeders: either mild hemophiliacs, with a chromosomal abnormality that means they lack necessary clotting factors; or with genetic abnormalities such as von Willebrand disease or Christmas disease, which cause clotting derangement. The true number of people with bleeding disorders—who have less than 40 percent of the clotting factor in their blood9—is unknown. Anyway, the figure is constantly changing, because for several years in the late 1970s and early 1980s, the factor that hemophiliacs were injecting came with HIV and hepatitis C in it. Hepatitis C, a blood-borne virus ten times as infectious as HIV, can be undetected for years and usually leads to cirrhosis and often cancer. A total of 4,689 hemophiliacs in the UK were infected with HIV and hepatitis C, of whom 2,883 have since died.10 That figure will be out of date by next week: because of the lag time, new cases are continually being diagnosed. A Westminster committee estimated that 32,718 people in the UK were infected with hepatitis C between 1970 and 1991 from contaminated blood products (including transfusions). Only 6,000 have been identified.11 Globally, 40,000 hemophiliacs have been infected with HIV from contaminated plasma products. No one yet knows how many got hepatitis C, but it is certainly hundreds of thousands.
Neil Weller, a hemophiliac from Oxfordshire, thinks he got off lightly. I met Neil through Facebook, which has become a hub for the rightly furious. The survivors, relatives, the grieving. In the UK alone there are campaigns named Contaminated Blood, Factor 8 Campaign, and Tainted Blood. Neil is cheery and chatty, his accent holding the rounded vowels of the west country that give a disconcerting warmth to statements such as: “I was eleven or twelve when I was told I didn’t have HIV.” But many of his friends did. Like most hemophiliacs, he spent much of his teenage years in and out of the hospital, dealing with bleeds. He remembers his fellow hemophiliacs there “and one by one they were told they had HIV and one by one they were going in another ward and they were dying.” When they died, the cause of death was given as pneumonia or something else. One friend, dead at thirty-two, left a two-year-old child. Another was a teenager. But Neil was fortunate, in his eyes: the contaminated plasma he had injected only gave him hepatitis C, a nasty chronic condition but not, as HIV was then, a certain killer. He walks with difficulty, but he is mobile, although he has had two knees replaced and his ankles are rotten. He has had twenty-two operations, including eighteen on his knees and ankles, and spent more than five hundred nights in the hospital. But he’s right: statistically, he is lucky.
Hemophilia is rotten. Hemophiliacs with no access to treatment usually die of bleeding to the brain or into the gut. This was always the case, no matter how much wealth and privilege they had: from Queen Victoria, the most famous transmitter of the faulty gene, hemophilia spread throughout the European royals, lovers of endemic intermarriage. The best-known royal hemophiliac, Tsarevich Alexei of Russia, would probably have died young had he not been shot first in a cellar in Ekaterinburg. Early death is the fate of hemophiliacs in most of the world, where treatment is expensive and rare. Dr. Mark Winter, a noted hemophilia expert, in 2017 recalled a recent visit to Pakistan where “they have got very nice hospitals, experienced doctors, good nurses, they are a nuclear power, but they have no [factor] concentrate.” Of the 250 children with severe hemophilia who attended the hemophilia center in Islamabad, he reported, only one lived beyond eighteen.12
Even with treatment, life for a hemophiliac was hard and frequently excruciating, but not in the way that most people think. It’s “that disease where if you cut yourself you bleed to death,” says Neil Weller, and I dare not tell him that that’s what I thought, before I began thinking better. Hemophiliacs bleed internally, frequently, and with violent pain. Justin Levesque is a severe hemophiliac who lives in Maine. He calls himself a “bleeder” and his license plate is “bruiser.” I asked him to describe the pain to me. This is an impossible request, as pain eludes description no matter how articulate you are. I try analogies. Is it like a broken leg? A burn? A stab wound? He first says, “The worst pain ever. Ever.” He tries again. “Your joint is an enclosed space, and then you’re trying to fill up a water balloon with as much water as you can but you can’t and it can’t pop either. It’s pressure and pain so you can’t think. The only thing I can relate it to is I had a kidney stone one time which was godawful, and it was pretty much on a par with that.” Other hemophiliacs say a bad bleed feels like a broken bone. We’re still in analogies and I can’t conceive of the pain until I see a severe hemophiliac walking: it is a twisted, unnatural movement, the legs stiffened into knock-kneed stilts. It looks like torment.
If a hemophiliac’s joint is knocked, blood vessels break. People with the more severe kind of hemophilia can also have spontaneous bleeds. Whatever the cause, there is then a “rush bleed,” because within twenty minutes, blood will have poured into the space surrounding a joint. Knees and ankles are most usually afflicted, but also fingers and elbows. The blood keeps flowing until there is no more space. The bones twist and move to accommodate the liquid. That is painful enough. Then the blood that shouldn’t be there presses on nerves, and that is agony. If this happens often, as it does with hemophiliacs, the affected joints deteriorate into arthritic ones. Rupert Miller, whose brother Julian was a severe hemophiliac, remembers his brother waking up all the family, screaming, night after night, in their farmhouse in Wales. All they could do was apply packs of frozen peas to his knees—the cold dulled the agony—and stay with him until the pain abated. The family freezer was filled with peas.
When Julian had a bad bleed, he sometimes went to the hospital. At that time, in the 1970s, the only treatment available was cryoprecipitate, a concentrated version of plasma with clotting factors. Hospitals were the safest place because cryo was difficult to prepare, requiring a freezer (then a rarity in British homes) and a complicated process of thawing and agitation. Julian was sometimes there for many weeks, many times a year. Once he missed two months of school. But his parents wanted him to be as normal as possible. Julian wanted to be as normal as possible and to attend the local school with his friends. He resisted going somewhere like Treloar College, a boarding school in Hampshire for disabled children, which had Gothic buildings, good care, and a dedicated hemophilia center.
In a BBC documentary, a former pupil named Ade Goodyear reminisced about life at Treloar.13 Being there didn’t fix your hemophilia, but if you felt the buzzing or tingling or heat that meant a bleed was coming, you could get treatment quickly and expertly. You never had to miss class again. Your schoolmates, unlike Goodyear’s at
his previous school, were unlikely to beat you up just to see what that did to a hemophiliac. (When Goodyear’s previous headmaster introduced him by saying, “You must not hit this boy,” his fate was fixed.) At Treloar there were thirty-five hemophiliac boys who knew what it was like. You weren’t judged. Treloar was a haven.
For every hemophiliac in the developed world, everything changed when Factor VIII arrived. Easy to prepare and relatively easy to infuse, it could even be used prophylactically, to prevent a bleed coming on. It was, says Rupert Miller, “wow.” Factor VIII was a revolution and a liberation. Factor, in the words of a public service video of the time, “is something that will let a hemophiliac live and bleed like a normal person.” For the first time, says Justin Levesque, hemophiliacs could have privacy. “They were going from being public, limping, being in the hospital, being very seen with their disorder, into the private.”
Cryoprecipitate was expensive. But so was this new Factor. The trouble was that one unit of plasma contains only a tiny amount of clotting factors. To be powerful enough, the concentrate had to come from a pool of thousands of donors. The higher the pool, the cheaper the processing costs and the greater the profit margin. This was a consideration, because the process of fractionation to create the new wonder drug was not cheap. Already, as soon as the new factors arrived—there was also Factor IX, for hemophilia B—some doctors were dubious. They knew that the larger the pool of plasma donors in each dose of concentrate, the higher the risk of infection. It was mathematics. In 1983, the vice president of Armour, a large US fractionator, testified to government that people who supplied the plasma for concentrate had it collected forty to sixty times a year. At that rate, “and given the pool sizes in the United States, four infected persons could contaminate the entire world supply of Factor VIII concentrate.”14