IELTS Academic Reading Practice Test 377

Measles is one of the most contagious diseases known to medicine. The virus travels through the air in droplets when an infected person coughs or sneezes, and it can remain suspended in a room for up to two hours after that person has left. Before a vaccine existed, infection was almost universal in childhood. In the United States alone, figures from the Centers for Disease Control and Prevention indicate that measles caused hundreds of deaths and tens of thousands of hospital admissions every year. A small but significant number of survivors were left with hearing loss or lasting damage to the brain. Worldwide, the virus still kills well over 100,000 people annually, most of them unvaccinated young children.

The scientist who did most to change this was John Franklin Enders, and little in his early life pointed towards medicine. Born in Hartford, Connecticut, in 1897, he graduated from Yale and then began graduate study in English literature at Harvard. He did not begin training in science until his late twenties, when an interest in infectious disease took him back to university. He completed a doctorate in bacteriology and immunology at Harvard in 1930 and remained at Harvard Medical School for the rest of his career, working in a laboratory at Boston Children's Hospital. He was patient, methodical and notably indifferent to publicity.

Enders came to virology at a time when most researchers assumed that viruses could be grown only in living animals or in fertilised hens' eggs. In 1949, with two younger colleagues, Thomas Weller and Frederick Robbins, he showed that poliovirus would multiply in test tubes containing tissue that was not of nervous origin. The finding made it possible to study viruses cheaply and safely, and it provided the foundation on which the first polio vaccines were later built. In 1954 the three men shared the Nobel Prize in Physiology or Medicine.

By then Enders had turned his attention to measles. The virus was known to be present in the blood of patients during the early, feverish stage of the illness, but no one had succeeded in keeping it alive outside the body. In 1954 a young colleague named Thomas Peebles obtained blood from a pupil at a boarding school in Massachusetts who had fallen ill with the disease. The boy was called David Edmonston, and Peebles carried the sample back to the laboratory. Under the microscope, infected cells could be seen clumping together into large multinucleated masses, a visible sign that the virus was multiplying and something not previously observed with measles.

The strain derived from that single sample became known as Edmonston, and it is the ancestor of most measles vaccines still in use. Enders's team then grew it again and again in cultures of monkey kidney cells and later in cells taken from chick embryos. This process, called passage, underlies almost every live viral vaccine. With each transfer to a fresh culture, the virus becomes better adapted to the cells in which it is grown and less able to cause disease in people. The change is gradual and unpredictable, and it took years of painstaking work, much of it carried out by a young researcher named Samuel Katz, to weaken the virus sufficiently for trials in children.

The first trials, from the late 1950s, showed that the weakened virus stimulated the immune system without producing a full attack of measles. The vaccine licensed in 1963, however, was far from perfect. Known as Edmonston B, it caused fever and a rash in a sizeable minority of children, and doctors often gave an injection of antibodies at the same time in order to soften the reaction. Later groups carried the attenuation further. A strain developed by Anton Schwarz produced far fewer side effects, and a still more attenuated preparation, Moraten, became the standard vaccine in the United States from 1968.

In countries that used the vaccine widely, the effect was dramatic. Reported measles cases in the United States fell from hundreds of thousands a year to a few thousand within two decades, and deaths from the disease became rare. In 1971 the vaccine was combined with those against mumps and rubella into a single injection, and the triple vaccine is now the usual means of protection in most wealthy countries. Two doses are recommended: the first at around twelve months, when the antibodies a baby acquires from its mother have faded, and the second before the child starts school.

Elsewhere progress has been uneven. Vaccination has brought deaths worldwide far below the level of 1980, when measles is estimated to have killed more than two million people, but the decline has stalled. The disease remains a leading cause of death among young children in low-income countries, and outbreaks have returned to wealthy ones where significant numbers of parents have declined immunisation. Interruption to routine vaccination during the COVID-19 pandemic left millions of children unprotected, and health agencies have warned that closing that gap will take years.

Enders continued to work at Boston Children's Hospital into his seventies, turning to other viruses, and he died in 1985. Measles was declared eliminated from the Americas in 2016, although outbreaks have since returned. For most of the world's children, the protection that began with a single blood sample in 1954 remains as necessary as ever.

Herd immunity, sometimes called herd protection, is the indirect defence that people who are not immune receive when a large enough share of the population around them is immune. When a virus enters such a population, most of the people it might have infected are already resistant, so each case gives rise to fewer new cases than the one before. Chains of transmission shrink and die out. The idea was described by epidemiologists early in the twentieth century, in studies of epidemics among laboratory animals, where an outbreak would fade once a certain proportion of the animals had survived infection. The principle is the same for vaccination: the more people who are protected, the less room the pathogen has to move.

How much protection is enough depends on how contagious the pathogen is. Epidemiologists express this with a quantity called the basic reproduction number, usually written R0. It is the average number of people whom a single infectious case would infect in a population where nobody has any immunity. A virus with an R0 of 3 will, on average, produce three new cases for each case. From this figure the herd immunity threshold can be estimated with a simple calculation: one minus one divided by R0. For an R0 of 3, that gives two-thirds, or about 67 per cent. These numbers are rough guides rather than precise targets, and they assume a population in which people mix at random.

Measles shows what a high threshold means in practice. Estimates of its R0 usually fall between 12 and 18, which implies that roughly 92 to 95 per cent of a population must be immune before transmission begins to fall. Campaigns in the Americas reached that level for a period, and the region was declared free of measles in 2016. When coverage slipped, however, the virus returned, and outbreaks have appeared in countries that had gone years without a case. Even a small fall below the threshold can be enough to allow several generations of transmission. No other common infection demands coverage so close to completeness.

The threshold is not, however, a wall that a population either reaches or does not. It is an average, and averages hide a great deal. People do not mix evenly. A city may have high overall coverage while a few neighbourhoods, schools or religious communities remain poorly vaccinated, and a virus introduced into one of those clusters will spread readily within it. Travel and close contact between young adults also matter, which is why outbreaks of measles and mumps have appeared on university campuses. A district that looks adequately covered on paper may contain a school where almost nobody is immunised. For this reason, public health specialists talk about pockets of susceptibility rather than a single national figure.

A further complication lies in what a vaccine actually does. Some vaccines prevent infection itself, a property immunologists call sterilising immunity: a vaccinated person who encounters the pathogen does not become infected and cannot pass it on. Others are less complete. They may protect the vaccinated individual from serious illness while allowing the virus to multiply in the nose and throat, so that person can still transmit it, often without noticing any symptoms. Several respiratory vaccines behave in this way to some degree. In such conditions, high coverage may reduce hospital admissions far more than it reduces transmission, and herd protection is weaker than the raw coverage figure suggests.

Protection can also fade. Antibody levels often decline over the months and years after vaccination or infection, and for some diseases this eventually leaves a person susceptible again. Memory cells of the immune system usually provide some lasting defence, which is why second attacks of many viruses are rare. Vaccines against mumps and pertussis, however, protect for a shorter time than their first trials suggested. Additional doses can restore antibody levels, and booster programmes are designed with exactly this decay in mind. How long protection lasts, and against which variant, remains one of the hardest questions in the field.

Where a disease is close to elimination, vaccination can be aimed at outbreaks rather than at whole populations. In ring vaccination, health workers identify each new case, trace everyone who has been in contact with that person and immunise them. The technique was central to the global campaign that eradicated smallpox, and it has been used more recently against Ebola. It suits infections that are rare, because contacts can be found and reached quickly, and it avoids the cost of mass campaigns. Its weakness is that it depends on detecting cases before the ring can be drawn around them.

Several things remain uncertain. Published estimates of R0 for the same pathogen can differ considerably, because they are calculated from data gathered in different settings. Immunity in a population is rarely measured directly. Coverage figures record doses delivered, not protection achieved, and they say nothing about how much of the vaccine was stored correctly or how well it worked in a particular group. Behaviour changes too. When people learn that an outbreak is under way they reduce their contacts, which lowers transmission and can make a pathogen look less contagious than it really is. None of this makes the concept useless, but it does mean that a threshold should be treated as a guide rather than a finishing line.

Closing a border is the most visible thing a government can do when a new infection appears. A ban on arrivals can be announced within hours, requires no hospital beds and gives the impression that the danger has been shut out. Restrictions are popular for precisely this reason: they appear to offer certainty in the face of a threat that is poorly understood. Yet the belief that a ban on arrivals can hold a virus at bay is among the most persistent and least examined assumptions in public health. The evidence for it is thinner than most ministers suppose.

That is not to say that such measures are worthless. Restrictions can genuinely buy time, and time is the resource a health system facing a new pathogen most lacks: weeks can be spent stocking wards, ordering tests and planning a vaccination campaign. For a small number of countries with few points of entry, closing borders may have delayed the arrival of infection for months. The argument of this article is therefore not that travel should never be restricted, but that restrictions are habitually oversold, rarely reviewed and often imposed in ways that punish the wrong people.

The evidence on how much time a ban actually buys is revealing. Modelling studies published in the first months of the COVID-19 pandemic examined the severe restrictions placed on movement out of Wuhan in January 2020. They suggested that those restrictions delayed the arrival of the virus in other Chinese cities by a few days. Its arrival in other countries, the same work indicated, was delayed by a few weeks at most. A delay of that length matters if it is used, but it is not the breathing space that the language of closing the borders implies. Once a virus is circulating widely within a country, restricting arrivals does almost nothing.

Checking travellers is equally disappointing. Screening at airports, whether by questionnaire or by measuring temperature, detects only a fraction of those carrying an infection. Many are incubating the virus and have no fever yet; others never develop symptoms at all and are nonetheless infectious. Studies of influenza and of COVID-19 have repeatedly found that entry screening catches very few cases, and that its main effect is to reassure the public. Quarantine of arrivals is a more substantial measure, but it is costly, difficult to enforce and, unless applied to all arrivals, no more complete than the testing on which it rests.

The costs, by contrast, are real. Border closures interrupt the movement of medical supplies, protective equipment and health workers, which is why the World Health Organization has generally advised against them during outbreaks of Ebola and other diseases. They strand citizens abroad, separate families and damage the livelihoods of people who work across frontiers. The damage falls most heavily on poorer countries, whose economies may depend on a handful of export industries and on remittances from workers overseas. A wealthy state can absorb the cost of a closed border for a year; a poor one may not be able to absorb it for a month.

International law tries to strike a balance. The International Health Regulations, revised in 2005, require countries to report outbreaks promptly and to share information, and they allow governments to impose additional measures such as screening or quarantine. Such measures must, however, be justified to the World Health Organization, must be proportionate to the risk and must be reviewed. During the COVID-19 pandemic many countries introduced restrictions that they never reported, and some were more severe than the situation could possibly justify.

Fairness is harder. A ban that singles out the nationals of one country, or the residents of one region, is difficult to defend on epidemiological grounds and easy to interpret as discrimination. When the Omicron variant was identified in southern Africa in late 2021, several governments banned travellers from the region within days. Officials at the World Health Organization responded sharply, pointing out that the countries being isolated were those that had done most to detect and report the variant. The likely effect, they suggested, would be to discourage others from looking as carefully.

What, then, should governments do? The alternative to a blanket ban is not inactivity but precision. Quarantine and testing of arrivals, applied consistently to everyone rather than to selected nationalities, are more effective and more defensible than closing a border to one passport. Restrictions can be limited to travellers from places where a variant is known to be circulating widely. They should also be reviewed at fixed intervals, since a measure introduced for a fortnight has a way of remaining in force for two years. Any restriction should be strictly limited in duration from the outset.

Travel restrictions are not, in the end, a wall against infection; at best they are a delay, and a short one. I would keep them available, because there are moments when a few weeks are worth a great deal. But I would treat them as one instrument among many, to be used with the same care as a drug that has serious side effects. They should be prescribed for a stated purpose, at a stated dose, and stopped when the purpose has been served.