IELTS Academic Reading Practice Test 378

On 5 June 1981 the Centers for Disease Control in Atlanta published a short report in its weekly bulletin. It described five young men in Los Angeles, all previously healthy, who had contracted a rare form of pneumonia usually seen only in patients whose immune systems had been destroyed by drugs or disease. Within weeks came reports of a similarly rare cancer, Kaposi's sarcoma, in young men in New York and California. Whatever was happening, the common factor appeared to be a collapse of the body's defences.

The syndrome had no name and no known cause. The following year the Centers for Disease Control adopted the term acquired immune deficiency syndrome, and surveillance was extended to the groups in which cases were accumulating: men who had sex with men, people who injected drugs, haemophiliacs who had received clotting factor, and migrants from Haiti. Hypotheses multiplied. Some researchers blamed a virus, others pointed to the immune overload supposedly caused by repeated infections, and others to recreational drugs. The virus theory gained ground only slowly.

In 1983 a team at the Pasteur Institute in Paris, led by Luc Montagnier and including Françoise Barré-Sinoussi, took a biopsy from the swollen lymph node of a patient. In the tissue they found evidence of a retrovirus, a class of virus that copies its genetic material into DNA. They called it lymphadenopathy-associated virus, or LAV, and published the finding in Science in May 1983. The result was tentative: the virus had been found in only a small number of patients, and proving that it caused the disease would take far more work.

Across the Atlantic, Robert Gallo's laboratory at the National Cancer Institute had studied retroviruses for years, and in 1984 his group reported isolating a virus from AIDS patients, which they named HTLV-III. On 23 April 1984 the American secretary of health, Margaret Heckler, called a press conference to announce that the cause of AIDS had been found and that a vaccine should be ready for testing within two years. No such vaccine existed then, and none has been licensed since — a reminder of how unreliable confident predictions can be.

It soon became clear that LAV and HTLV-III were the same agent, and the quarrel over who had found it turned bitter, with accusations of misappropriated samples and rival claims to priority. In 1987 the two governments agreed that the credit, and the royalties from the blood test, should be shared. The argument resurfaced in 2008, when Montagnier and Barré-Sinoussi received the Nobel Prize in Physiology or Medicine and Gallo did not. By then the naming had long been settled: in 1986 an international committee had given the virus the name by which it is now known, human immunodeficiency virus.

Diagnosis was transformed in March 1985, when the first commercial test for antibodies to the virus was licensed in the United States. Within months blood banks were screening donations, which sharply reduced transmission through transfusion in countries that could afford to test. The test also made it possible, for the first time, to estimate how many people were infected. But antibodies take weeks to appear, so early infection remained invisible; the gap is now closed by tests that detect the virus itself.

Treatment lagged behind. The first drug to be approved was azidothymidine, or AZT, a compound synthesised in the 1960s as a possible anticancer agent and then abandoned. It belongs to a class known as nucleoside analogues, which mimic the building blocks of DNA and bring the copying of viral genetic material to a halt. A controlled trial reported in 1986 was stopped early because patients taking the drug were dying at a lower rate than those on placebo, and the Food and Drug Administration approved it in March 1987.

AZT was not a cure. The doses first used were high, and they damaged bone marrow, so that many patients needed blood transfusions; later work showed that much lower doses worked as well with fewer side effects. The drug was also expensive. More troubling still, in 1994 a large Anglo-French study called Concorde reported that starting AZT immediately, rather than waiting for symptoms, gave no survival advantage over several years. A single drug, it seemed, bought time but could not hold the virus back for long.

The explanation lay in the way the virus replicates. Researchers showed that HIV produces enormous numbers of new particles every day and that its copying enzyme makes frequent mistakes, so resistant variants arise readily and one drug merely selects them. In 1996, at an international conference in Vancouver, several teams reported that combinations of three drugs, including a new class called protease inhibitors, could reduce the amount of virus in the blood below the limit of detection. Deaths from AIDS in wealthy countries fell sharply over the next two years.

Combination therapy turned HIV from a fatal illness into a manageable chronic condition for those who could obtain it. In much of Africa, where the burden was heaviest, it stayed out of reach for years: the cost ran to many thousands of dollars per patient annually, and prices fell only after generic manufacturers began supplying copies and a World Trade Organization declaration in 2001 affirmed the right of countries to override patents in a public health emergency. Even now, no treatment removes the virus from the body, and patients must take tablets for life.

A virus is not a cell. It consists of genetic material — DNA or RNA — wrapped in a protein coat, and sometimes in an outer envelope of lipid. It has no metabolism of its own, cannot generate energy and cannot make proteins. To reproduce, it must attach to a living cell, insert its genes and force the cell's own machinery to manufacture viral components. This absolute dependence is what makes viral infections so difficult to treat. A drug that blocked the machinery of the virus would often block the machinery of the patient too, so antiviral drugs must aim at the small number of steps and structures that are unique to the virus.

HIV provides the clearest illustration of how many such steps there are. The virus infects cells of the immune system that carry a surface protein called CD4, principally helper T cells. It attaches to CD4 and to a second receptor, usually CCR5 or CXCR4, then fuses its envelope with the cell membrane and releases its contents. An enzyme called reverse transcriptase copies the viral RNA into DNA, which is carried into the nucleus and inserted into the cell's own genome by another enzyme, integrase. There it may remain silent for years.

When the cell is activated, it reads the viral genes and produces long chains of protein that must be cut into functional pieces by a third enzyme, protease, before new particles can assemble and bud from the surface. Each of these steps has been turned into a drug target, and each class of drug is named after the step it blocks: entry inhibitors, reverse transcriptase inhibitors, integrase inhibitors and protease inhibitors. The first effective drugs, such as AZT, were nucleoside analogues — molecules sufficiently similar to the natural building blocks of DNA that reverse transcriptase incorporates them and then cannot continue.

The principle behind these drugs is selective toxicity. Because reverse transcriptase, protease and integrase are viral enzymes with no close human equivalent, blocking them damages the virus far more than the patient. Even so, side effects are common. Nucleoside analogues can affect mitochondria, the energy-producing structures inside cells, which helps to explain some of the fatigue and the liver and kidney problems associated with long-term use. Modern regimens use lower doses and better-tolerated drugs than the earliest trials, but antiviral treatment still requires regular blood tests.

Combination therapy rests on arithmetic. HIV replicates at an extraordinary rate, and its reverse transcriptase has no proofreading mechanism, so errors accumulate and mutations are constantly generated. A single mutation may make the virus resistant to one drug. The chance that one particle will simultaneously carry the mutations needed to defeat three drugs is very small, so a regimen of three drugs from different classes suppresses the virus far more durably than any single drug could. When the virus is suppressed to undetectable levels, transmission to sexual partners is effectively eliminated — the basis of the campaign known as undetectable equals untransmittable.

The same logic applies to other viruses, with different targets. Aciclovir, used against herpes, is a striking example of selectivity: it is activated by a viral enzyme, thymidine kinase, and therefore becomes toxic mainly inside infected cells. Influenza viruses are released from a cell with the help of an enzyme called neuraminidase, and drugs such as oseltamivir block it, although they must be given within about two days of the first symptoms to shorten the illness appreciably. For hepatitis C, combinations of direct-acting antivirals can now cure more than nine out of ten patients.

Not every virus offers such targets. Some, including the many viruses that cause the common cold, vary so much and are so numerous that a single drug is impractical. Others establish latency, hiding in cells where drugs cannot reach them. HIV is the best-known case: even after decades of treatment a small reservoir of infected memory T cells persists, and if therapy stops the virus returns within weeks. Eliminating that reservoir is the central obstacle to a cure, and the strategies under investigation — waking the dormant virus so that the immune system can destroy it, editing the genes of infected cells, or using antibodies that neutralise a wide range of strains — have so far produced only isolated successes.

Antivirals also work best when given early, before the virus has multiplied widely and before the immune response has done collateral damage. This is straightforward for influenza, where the illness announces itself quickly, but far harder for HIV, whose acute phase is easily mistaken for flu. It is one reason why testing matters: a diagnosis made in time allows treatment to begin while the immune system is still intact, and the earlier the treatment, the less damage the body sustains.

Resistance remains the constant threat. Because resistant mutants can exist before treatment starts, and because patients occasionally miss doses, a regimen fails when the virus is exposed to a single drug for long enough to adapt. Surveillance programmes therefore track the mutations circulating in a population, and guidelines change as they spread. The history of amantadine, an early influenza drug, is instructive: resistant strains became so common that it is no longer recommended. Access is the other persistent problem; in many low-income countries, antiviral treatment still arrives later and reaches fewer people than in rich ones.

Two decades ago, the idea that a healthy person could take a pill every day to avoid infection with HIV sounded fanciful. Today it is standard practice in many countries. Pre-exposure prophylaxis, or PrEP, involves taking antiretroviral drugs before exposure rather than after, and the evidence that it protects the great majority of consistent users is now substantial. What remains genuinely contested is not whether PrEP should exist but who should pay for it. The question is usually framed as a simple matter of health economics; in truth it is a question about what kind of society we want.

The drugs involved are the same ones used to treat HIV, chiefly a combination of tenofovir and emtricitabine. In July 2012 the Food and Drug Administration approved that combination for prevention in the United States, and in 2015 the World Health Organization recommended that people at substantial risk of infection should be offered it. The Centers for Disease Control and Prevention estimates that consistent use reduces the risk of sexual transmission by around 99 per cent. The qualification matters: protection depends on the drug being present in the body, and in several trials effectiveness was far lower because participants did not take it regularly.

The case for providing PrEP without charge to the user rests on two arguments, one economic and one moral. The economic argument is that prevention is cheap by comparison with treatment. A lifetime of antiretroviral therapy, clinic visits and monitoring costs hundreds of thousands of dollars; a year's supply of generic PrEP costs a small fraction of that sum. The moral argument is that a charge deters precisely the people who most need the drug. When a month's supply costs more than a low-paid worker earns in a week, those at greatest risk — young men, migrants, people without stable housing — are the least likely to buy it.

Critics reply that free provision removes the incentive to avoid infection. If the state pays for the pill, the argument runs, people will abandon condoms and take risks they would otherwise shun. This is a testable claim, and the evidence is mixed but not damning. Studies of PrEP users have generally found little sign of a large increase in unprotected sex, and diagnoses of other sexually transmitted infections have risen among users partly because they are tested every few months, something few of their peers do. It would be odd, in any case, to withhold a medicine on the ground that its recipients might behave badly.

The dispute has been sharpest where public money is short. In England, the National AIDS Trust, a charity, took NHS England to court in 2016 after the health service argued that it had no legal power to commission PrEP; the courts disagreed, and a publicly funded trial followed, with routine commissioning beginning in October 2020. Scotland had acted earlier, making PrEP available on its health service from 2017. The delay was not merely bureaucratic: during the years of argument, infections occurred that could have been prevented.

Health economists add a further complication. Budgets are usually separated into prevention and treatment, and a manager who funds PrEP from a prevention budget saves money for a different budget entirely. The savings are real, but they accrue elsewhere, which is why cost-effectiveness analyses, however favourable, do not always persuade the people who hold the purse strings. A drug that prevents an expensive illness ought to be attractive to any insurer; a system that cannot count the benefit often fails to see it.

There is also the question of targeting. No country proposes offering PrEP to everyone. The choice is between a service that is free at the point of use for anyone who asks, and one that requires a clinician or an online questionnaire to judge whether the applicant is at sufficient risk. The second sounds prudent, but in practice it excludes people who do not recognise themselves in the categories, including many women and older people, whose risk is rising in several countries. Means-testing, meanwhile, produces the worst of both worlds: a bureaucracy that costs money to run and a charge that still deters.

None of this means that free PrEP should be unconditional. A responsible programme offers the drug only alongside regular testing for HIV and other infections, because starting PrEP while already infected risks breeding resistance, and because the three-monthly check-up is the moment when other problems can be caught. It should be easy to obtain, from pharmacies and clinics without a referral from a family doctor, and it should be monitored so that money follows evidence rather than habit.

My conclusion is therefore straightforward. Drugs that prevent HIV should be free to the user, paid for collectively, and offered without moral inspection to anyone at risk. The objection that this subsidises irresponsibility belongs to an older argument about illness, one that treated infection as a punishment and ignored the fact that nobody chooses to be exposed to a virus. Prevention that depends on the ability to pay is not a public health policy; it is a lottery with a known list of losers.