TheChek News Flow

The President’s mendacious nightly press briefings on the coronavirus will go down in history for their monumental flimflammery.

uring the Vietnam War, the United States had the Five O’Clock Follies, nightly briefings at which American military leaders claimed, citing a variety of bogus statistics, half-truths, and misleading reports from the front, to be winning a war that they were, in fact, losing. Richard Pyle, the Associated Press’s Saigon bureau chief, called the press conferences “the longest-playing tragicomedy in Southeast Asia’s theater of the absurd,” which, minus the “Southeast Asia” part, is not a bad description of the scene currently playing out each evening in the James S. Brady Press Briefing Room, in the White House. We now have the Trump Follies, the nightly briefings at which President Trump has lied and bragged, lamented and equivocated, about the global pandemic that poses an existential threat to his Presidency. Just as the Vietnam briefings became a standard by which the erosion of government credibility could be measured then, historians of the future will consult the record of Trump’s mendacious, misleading press conferences as an example of a tragic failure of leadership at such a critical moment. There will be much material for them; the transcripts from just the first three days of this week runs to more than forty thousand words.

Since Trump began making the press conferences a daily ritual a couple of weeks ago—an eternity in the pandemic era—his more memorable lines are already featuring in political attacks against him. “I don’t take responsibility at all,” Trump insisted, two weeks ago. When asked to assess his own performance, he said, “I’d rate it a ten.” This Wednesday, with members of his coronavirus task force joining him onstage, he added, “We’ve done one hell of a job. Nobody has done the job that we’ve done. And it’s lucky that you have this group here right now for this problem or you wouldn’t even have a country left.”

The disconnect between Trumpian reality and actual reality has never been on starker display than in the past few days, as the true face of the horror we are facing in the United States has shown itself, in New York City, with overwhelmed morgues and emergency rooms, a governor pleading for ventilators and face masks from the federal government, and heartbreaking first-person accounts reminiscent of the open letters sent from Italy a few weeks back, which warned Americans: this is what is coming for you—don’t make our mistakes. On Tuesday, the World Health Organization said that the United States was emerging as the “epicenter” of the global pandemic, which makes the James S. Brady Press Briefing Room the emerging epicenter of the failure to respond to it.

A couple of weeks ago, it seemed as if maybe that would not be the case. Although the Trump Administration had faltered and delayed and denied through the initial stages of the virus, when it raged outside our borders, it looked like it might finally get its act together and take this public-health menace seriously, now that it was hitting in force inside the U.S. Trump declared a “national emergency,” stepped up testing, and, on March 16th, agreed to his crisis committee’s plan for a fifteen-day countrywide slowdown, in order to “flatten the curve” of the disease’s trajectory. Barely a week into the fifteen days, however, Trump began signalling an abrupt change of course—at just the moment when the disease was accelerating its deadly progress through a wealthy nation that turned out to be surprisingly ill-prepared for it.

Throughout this long, strange March, Trump has often framed the fight against the pandemic in martial terms: a “battle” to be won, a victory to be achieved, a shared sacrifice against “this invisible enemy” which would go on “until we have defeated the virus.” But the Commander-in-Chief did something extraordinary this week: he rebelled against his own clichés, essentially declaring that he no longer wanted to be at war with the virus after all.

On Sunday, he prefigured this pivot, apparently after watching the Fox News host Steve Hilton complain about the treatment—a shut-down country and a cratered economy—being worse than the disease. “WE CANNOT LET THE CURE BE WORSE THAN THE PROBLEM ITSELF,” Trump tweeted, shortly before midnight. By the Monday-night edition of the Follies, which are usually scheduled for 5 p.m. but often not started until later, Trump was repeating this line over and over again. “We cannot let the cure be worse than the problem itself,” he said. “We’re not going to let the cure be worse than the problem.” Later, he added, “We can’t have the cure be worse than the problem,” and also, “We can’t let that happen. . . . We can’t let this continue to go on.” America, he said, would be “open for business” soon.

On Tuesday, which marked a month since a now-infamous tweet in which the President claimed that “the Coronavirus is very much under control in the USA,” Trump was even more specific. He announced that afternoon, on a Fox News special from the White House lawn, that he wanted to get the country reopened and the church pews “packed” by Easter, on April 12th, at just the time when New York and other states were predicted to face the maximum pressure on their overstretched medical facilities. A few hours later, at the nightly press briefing, he was asked about this seemingly arbitrary timetable by CNN’s Kaitlan Collins.

“Who suggested Easter?” Collins asked. “Who suggested that day?” Trump replied, “I just thought it was a beautiful time. It would be a beautiful time, a beautiful timeline. It’s a great day.” Collins followed up: “So that wasn’t based on any of the data?” “I just think it would be a beautiful timeline,” Trump responded.

We’ve counted the viral spread across peoples; now we need to count it within people.

In the third week of February, as the covid-19 epidemic was still flaring in China, I arrived in Kolkata, India. I woke up to a sweltering morning—the black kites outside my hotel room were circling upward, lifted by the warming currents of air—and I went to visit a shrine to the goddess Shitala. Her name means “the cool one”; as the myth has it, she arose from the cold ashes of a sacrificial fire. The heat that she is supposed to diffuse is not just the fury of summer that hits the city in mid-June but also the inner heat of inflammation. She is meant to protect children from smallpox, heal the pain of those who contract it, and dampen the fury of a pox epidemic.

The shrine was a small structure within a temple a few blocks from Kolkata Medical College. Inside, there was a figurine of the goddess, sitting on a donkey and carrying her jar of cooling liquid—the way she has been depicted for a millennium. The temple was two hundred and fifty years old, the attendant informed me. That would date it to around the time when accounts first appeared of a mysterious sect of Brahmans wandering up and down the Gangetic plain to popularize the practice of tika, an early effort at inoculation. This involved taking matter from a smallpox patient’s pustule—a snake pit of live virus—and applying it to the pricked skin of an uninfected person, then covering the spot with a linen rag.

The Indian practitioners of tika had likely learned it from Arabic physicians, who had learned it from the Chinese. As early as 1100, medical healers in China had realized that those who survived smallpox did not catch the illness again (survivors of the disease were enlisted to take care of new victims), and inferred that the exposure of the body to an illness protected it from future instances of that illness. Chinese doctors would grind smallpox scabs into a powder and insufflate it into a child’s nostril with a long silver pipe.

Vaccination with live virus was a tightrope walk: if the amount of viral inoculum in the powder was too great, the child would succumb to a full-fledged version of the disease—a disaster that occurred perhaps one in a hundred times. If all went well, the child would have a mild experience of the disease, and be immunized for life. By the seventeen-hundreds, the practice had spread throughout the Arab world. In the seventeen-sixties, women in Sudan practiced tishteree el jidderee (“buying the pox”): one mother haggling with another over how many of a sick child’s ripe pustules she would buy for her own son or daughter. It was an exquisitely measured art: the most astute traditional healers recognized the lesions that were likely to yield just enough viral material, but not too much. The European name for the disease, variola, comes from the Latin for “spotted” or “pimpled.” The process of immunizing against the pox was called “variolation.”

Lady Mary Wortley Montagu, the wife of the British Ambassador to Constantinople, had herself been stricken by the disease, in 1715, leaving her perfect skin pitted with scars. Later, in the Turkish countryside, she witnessed the practice of variolation, and wrote to her friends in wonder, describing the work of one specialist: “The old woman comes with a nut-shell full of the matter of the best sort of small-pox, and asks what vein you please to have opened,” whereupon she “puts into the vein as much matter as can lie upon the head of her needle.” Patients retired to bed for a couple of days with a fever, and, Lady Montagu noted, emerged remarkably unscathed. “They have very rarely above twenty or thirty in their faces, which never mark; and in eight days’ time they are as well as before their illness.” She reported that thousands safely underwent the operation every year, and that the disease had largely been contained in the region. “You may believe I am well satisfied of the safety of this experiment,” she added, “since I intend to try it on my dear little son.” Her son never got the pox.

In the centuries since Lady Montagu marvelled at the efficacy of inoculation, we’ve made unimaginable discoveries in the biology and epidemiology of infectious disease, and yet the covid-19 pandemic poses no shortage of puzzles. Why did it spread like wildfire in Italy, thousands of miles from its initial epicenter, in Wuhan, while India appears so far to have largely been spared? What animal species transmitted the original infection to humans?

But three questions deserve particular attention, because their answers could change the way we isolate, treat, and manage patients. First, what can we learn about the “dose-response curve” for the initial infection—that is, can we quantify the increase in the risk of infection as people are exposed to higher doses of the virus? Second, is there a relationship between that initial “dose” of virus and the severity of the disease—that is, does more exposure result in graver illness? And, third, are there quantitative measures of how the virus behaves in infected patients (e.g., the peak of your body’s viral load, the patterns of its rise and fall) that predict the severity of their illness and how infectious they are to others? So far, in the early phases of the covid-19 pandemic, we have been measuring the spread of the virus across people. As the pace of the pandemic escalates, we also need to start measuring the virus within people.

Most epidemiologists, given the paucity of data, have been forced to model the spread of the new coronavirus as if it were a binary phenomenon: individuals are either exposed or unexposed, infected or uninfected, symptomatic patients or asymptomatic carriers. Recently, the Washington Post published a particularly striking online simulation, in which people in a city were depicted as dots moving freely in space—uninfected ones in gray, infected ones in red (then shifting to pink, as immunity was acquired). Each time a red dot touched a gray dot, the infection was transmitted. With no intervention, the whole field of dots steadily turned from gray to red. Social distancing and isolation kept the dots from knocking into one another, and slowed the spread of red across the screen.

This was a bird’s-eye view of a virus radiating through a population, seen as an “on-off” phenomenon. The doctor and medical researcher in me—as a graduate student, I was trained in viral immunology—wanted to know what was going on within the dots. How much virus was in that red dot? How fast was it replicating in this dot? How was the exposure—the “touch time”—related to the chance of transmission? How long did a red dot remain red—that is, how did an individual’s infectiousness change over time? And what was the severity of disease in each case?

What we’ve learned about other viruses—including the ones that cause aids, sars, and smallpox—suggests a more complex view of the disease, its rate of progression, and strategies for containment. In the nineteen-nineties, as researchers learned to measure how much H.I.V. was in a patient’s blood, a distinct pattern emerged. After an infection, the virus count in the blood would rise to a zenith, known as “peak viremia,” and patients with the highest peak viremia typically became sicker sooner; they were least able to resist the virus. Even more predictive than the peak viral load was the so-called set point—the level at which someone’s virus count settled after its initial peak. It represented a dynamic equilibrium that was reached between the virus and its human host. People with a high set point tended to progress more rapidly to aids; people with a low set point frequently proved to be “slow progressors.” The viral load—a continuum, not a binary value—helped predict the nature, course, and transmissibility of the disease. To be sure, every virus has its own personality, and H.I.V. has traits that make viral load especially revealing: it causes a chronic infection, and one that specifically targets cells of the immune system. Yet similar patterns have been observed with other viruses.

And, immunologically, that’s not surprising. If your system is able to combat viral replication with some efficiency—owing to your age, your genetics, and other indices of immune competence—you’ll have a lower set point. Could a lower initial exposure, as with children treated with tika, also lead to a lower set point? Faced with a smaller challenge, the immune system could have a greater chance of controlling the pathogen. In contrast, if you’re inundated with multiple high-dose exposures, the swiftly replicating invader could gain ground that the immune system might be hard-pressed to reconquer.

An ingenious study on the relationship between the intensity of viral exposure and infectivity in human beings comes from a team at the Fred Hutchinson Cancer Research Center and the University of Washington, in Seattle. In 2018, an epidemiologist and statistician named Bryan Mayer joined a group of physicians and biologists who were researching a problem that seemed, on its face, almost impossible to tackle. Mayer, who is in his mid-thirties, is soft-spoken and precise: he uses words carefully, and speaks in long, slow sentences. “Even as a graduate student, I was interested in the idea of a dose of a virus or a pathogen,” he told me. “But the problem is that the initial dose is often impossible to capture, because you only know a person is infected after he or she has been infected.” Most infectious diseases can only be viewed in a rearview mirror: by the time a patient becomes a patient, that critical moment of transmission has already passed.

But the researchers found an unusual resource: a cohort of new mothers and their children in Kampala, Uganda. A few years earlier, a pediatrician named Soren Gantt and a team of doctors examined these women, and asked them to provide oral swabs for a year. Then they measured how much the women shed a virus called HHV-6, which is usually spread through oral secretions to an infant after birth, and which causes fever and a red whole-body rash. It was now possible to investigate how the amount of virus-shedding—the “dose” of exposure—affected the likelihood of a newborn infant becoming infected. Gantt, Mayer, and their colleagues had devised a way to eavesdrop on the dynamics of the transmission of a human viral infection from the very start. “Our data confirmed that there’s a dose-response relationship in viral transmissions for HHV-6,” Mayer told me. “The more virus you shed, the more likely you are to infect others.” He’d managed to turn around the rearview mirror of epidemiology.

There’s another aspect of transmission and disease, however: the host immune response. Viral attack and the immune system’s defense are two opposing forces, constantly at odds. The Russian immunologist Ilya Metchnikoff, working in the early nineteen-hundreds, described the phenomenon as “the struggle”—or Kampf, in German editions of his work. Metchnikoff imagined an ongoing battle between microbe and immunity. The Kampf was a matter of ground gained or lost. What was the total “force” of the microbial presence? What host factors—genetics, prior exposure, baseline immune competence—were limiting the microbial invasion? And then: was the initial equilibrium tipped toward the virus, or toward the host?

That raises the second question—does a larger viral “dose” result in more severe disease? It’s impossible to erase from one’s memory the image of Li Wenliang, the thirty-three-year-old Chinese ophthalmologist who sounded the alarm on the first covid-19 cases, in his final illness; a photograph shows him crimson-faced, sweating, and struggling to breathe in a face mask, shortly before his death. Then there’s the unexpected death of Xia Sisi, a twenty-nine-year-old doctor from Union Jiangbei Hospital of Wuhan, who had a two-year-old child and, the Times reported, loved Sichuan hot pot. Another Chinese health-care worker, a twenty-nine-year-old nurse in Wuhan, fell so critically ill that she started hallucinating; later, she would describe herself as “walking on the edge of death.”

Could the striking severity of their disease—twenty- and thirty-year-olds with covid-19 generally experience a self-limited, flu-like illness—be correlated with the amount of virus to which they were initially exposed? At least two E.R. doctors in the United States, both on the front lines of the pandemic, have also fallen critically ill; one of them, in Washington State, is only in his forties. To go by available data from Wuhan and Italy, health-care workers don’t necessarily have a higher fatality rate, but do they suffer, disproportionately, from the most severe forms of the disease? “We know the high mortality in older people,” Peter Hotez, an infectious-disease specialist and vaccine scientist at Baylor College of Medicine, told CNN. “But, for reasons that we don’t understand, front-line health-care workers are at great risk for serious illness despite their younger age.”

Some suggestive research has been done with other viruses. In animal models of influenza, it’s possible to precisely quantify exposure intensity, and mice who were given higher doses of certain influenza viruses developed a more severe form of the disease. Yet the degree of correlation between dose and disease severity varied widely from one strain of the flu to the next. (Curiously, in one study a higher initial load of respiratory syncytial virus, which can cause pneumonia, especially in young children, correlated negatively with severe disease—although another study suggests that the correlation is positive with toddlers, the most affected patient population.)

What sparse evidence we have about coronaviruses suggests that they may follow the pattern seen in influenza. In a 2004 study of the coronavirus that causes sars, a cousin of the one that causes covid-19, a team from Hong Kong found that a higher initial load of virus—measured in the nasopharynx, the cavity in the deep part of your throat above your palate—was correlated with a more severe respiratory illness. Nearly all the sars patients who came in initially with a low or undetectable level of virus in the nasopharynx were found at a two-month follow-up to be still alive. Those with the highest level had a twenty- to forty-per-cent mortality rate. This pattern held true regardless of a patient’s age, underlying conditions, and the like. Research into another acute viral illness, Crimean-Congo hemorrhagic fever, reached a similar conclusion: the more virus you had at the start, the more likely you were to die.

Perhaps the strongest association between the intensity of exposure and the intensity of subsequent disease is seen in measles research. “I want to emphasize that measles and covid-19 are different diseases caused by very different viruses with different behaviors,” Rik de Swart, a virologist at Erasmus University, in Rotterdam, cautioned when we spoke, “but in measles there are several clear indications that the severity of illness relates to the dose of exposure. And it makes immunological sense, because the interaction between the virus and the immune system is a race in time. It’s a race between the virus finding enough target cells to replicate and the antiviral response aiming to eliminate the virus. If you give the virus a head start with a large dose, you get higher viremia, more dissemination, higher infection, and worse disease.”

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He described a study from 1994 in which researchers gave monkeys different doses of the measles virus and found that higher infection doses were associated with earlier peaks in viremia. In human beings, de Swart added, the best evidence comes from studies in sub-Saharan Africa. “If you acquire measles through household contacts, where the density and dose of exposure is the highest—you might be sharing a bed with an infected child—then you typically have a higher risk of developing more severe illness,” he said. “If a child contracts the disease through playground or casual contact, the disease is usually less severe.”

I discussed this aspect of infection with the Harvard virologist and immunologist Dan Barouch, whose lab is among those that are working toward a vaccine against sars-CoV-2, the virus that causes covid-19. He told me that ongoing studies with macaques are investigating the relationship between the initial dose of the sars-CoV-2 viral inoculum and the amount of virus in lung secretions at a later time. He believes that there may be a correlation. “If we extended this logic to humans, we would expect a similar relationship,” he said. “And, logically, the larger amount of virus should trigger more severe disease by prompting a brisker inflammatory response. But that is still speculative. The relationship between initial viral dose and severity remains to be seen.”

To answer the third question—whether we can track a covid-19 patient’s viral load in a way that helps us predict the course of the disease—we’ll need more quantitative research into sars-CoV-2 counts within patients. One unpublished German study has measured viral loads on oral swabs taken of both symptomatic and asymptomatic individuals. Initially, it was reported that patients who experienced no symptoms had slightly higher loads than those who fell ill. The results were curious. But at the time only seven patients had been studied. Sandra Ciesek, the director of the Institute of Medical Virology, in Frankfurt, who was running the study, told me that no significant differences between the two groups emerged as a larger patient population began to be sampled. “In swabs, we don’t know of a correlation,” she informed me. The problem with measuring viral loads in a swab is that it is “affected by preanalytic factors, such as the way in which the swab is taken,” she added. Oral swabs are notoriously affected by small variations in how they’re done. “But a correlation with severe disease may well be true for the viral load in blood.” Joshua Schiffer, a clinical virologist at the Fred Hutchinson Center, and a co-author of the HHV-6 study, reports that more stringent nasal-swabbing methods for a range of respiratory viruses have yielded consistent, reliable viral-load counts, and that these loads have generally tracked well with disease symptoms and progression. In a paper published online by The Lancet Infectious Diseases in March, researchers at the University of Hong Kong and Nanchang University reported that viral loads in nasopharyngeal swabs from a group of patients with severe covid-19 were sixty times higher, on average, than the loads among patients with a mild form of the disease.

As the virus continues to cyclone across the world, we will begin to find quantitative answers to these questions of how exposure intensity and subsequent viral loads relate to the clinical course of covid-19. We will supplement the bird’s-eye view with the worm’s-eye view. How will these insights change the way we manage patients, hospitals, and populations?

Start with the relationship between exposure intensity and infection. Think, for a moment, of how we monitor those who work with radiation. Using radiation dosimetry, we quantify someone’s total exposure, and we set limits on it. We already know how critical it is for doctors and nurses to limit exposure to the coronavirus by using protective equipment (masks, gloves, gowns). But for health-care workers on the front lines of the covid-19 pandemic, especially in places where protective equipment is scarce, we might also keep track of total exposure, and put in place viral-dosimetry controls, so that one individual can avoid repeated interactions with some set of highly contagious patients.

Establishing a relationship between dose and disease severity could, in turn, affect patient care. If we could identify pre-symptomatic patients who were likely exposed to the highest doses of viruses—someone cohabitating or socializing with multiple sick family members (as with the close-knit Fusco family of Freehold, New Jersey, which has had four deaths), or a nurse exposed to a set of patients shedding large amounts of the virus—we might predict a more severe experience of the disease, and give them priority when it came to limited medical resources, so that they could be treated faster, earlier, or more intensively.

And, finally, the care of covid-19 patients could change if we began to track virus counts. These parameters could be gauged using fairly inexpensive and easily available laboratory methods. Imagine a two-step process: first, identifying infected patients, and then quantifying viral loads in nasal or respiratory secretions, particularly in patients who are likely to require the highest level of treatment. Correlating virus counts and therapeutic measures with outcomes might result in different strategies of care or isolation.

The value of a quantitative approach applies to clinical studies as well. Clinical drug trials are typically more informative when run on subjects who aren’t yet critical; once the subjects have reached that stage, any therapy might be too little, too late. And if the disease course in such patients is followed using viral-load metrics, rather than by tracking symptoms alone, the effect of a drug in different trials can be compared more easily and accurately.

We will also want to be able to identify people who have recovered from infection, have become immune to sars-CoV-2, and are no longer contagious. Such people must meet two criteria: they must have a measured absence of viral shedding, and they must have signs of persistent immunity in their blood (something readily determined by an antibody test). As the Chinese discovered with smallpox in the twelfth century, such individuals—especially those who are health-care workers—are of particular value to medicine: barring any decay in immunity, they can generally tend to the sickest patients without getting sick themselves.

My clinical practice is in oncology. Measurement and enumeration are the mainstays of medicine for people in my field: the size of a tumor, the number of metastases, the exact shrinkage of a malignant mass after chemotherapy. We talk about “risk stratification” (categorizing patients according to health status) and the “stratification of response” (categorizing patients according to their response to treatment). I am able to spend half an hour or more with every patient to describe risk, explain how a remission is measured, and carefully devise a clinical plan.

A pandemic, by contrast, goes hand in hand with panic. Chaos reigns. Italian doctors are hanging I.V. drips on makeshift poles for patients lying on makeshift cots in makeshift wards. Measurement—viral-load testing—can seem like an improbable indulgence under such circumstances. But this crisis will require that we stratify and assess risk, and deploy dwindling resources in the most effective manner.

The word “epidemiology” is derived from “epi” and “demos”—“above the people.” It is the science of aggregation, the science of the many. Yet it works most effectively when it moves in step with medicine, the science of the one. On the morning I visited the Shitala shrine in Kolkata, the goddess of bygone population-decimating epidemics was also serving as the personal goddess of a mother who had brought a child with a weeklong fever. To win the Kampf against covid-19, it’s essential to trace the course of the virus as it moves through populations. But it’s equally essential to measure its course within a single patient. The one becomes the many. Count both; both count. ♦

Phone call signals potential thaw after countries traded barbs over pandemic

Donald Trump and Xi Jinping spoke by telephone on Friday, signalling a potential thaw in relations between the world’s two most powerful countries after weeks of bitter exchanges over the coronavirus pandemic.

In a tweet, the US president described his first interaction with his Chinese counterpart since the outbreak began three months ago as “very good”.

“China has been through much [and] has developed a strong understanding of the Virus,” Mr Trump added. “We are working closely together. Much respect!”

Chinese state media said that Mr Xi had spoken with Mr Trump “at the invitation of the US side”, and offered to “unreservedly share [China’s] experience in prevention and control efforts, and treatment with the World Health Organization and countries including the US”.

Over recent days, Mr Trump has stopped referring to the coronavirus as “the Chinese virus”, which had angered officials in Beijing and triggered domestic criticism that he was stoking anti-Asian sentiment as the virus spread rapidly across the US.

US officials countered that the designation was fair in light of some Chinese diplomats’ endorsement of unproven conspiracy theories blaming the US military for the outbreak, which began in the central Chinese city of Wuhan in December or November.

However, other senior Trump administration officials were continuing to insist that the virus should be referred to as “the Wuhan coronavirus”.

The war of words threatened to impede any prospects of meaningful co-operation between the US and China as the pandemic continued to spread rapidly around the world. It also coincided with a charm offensive by Beijing heralding its dispatch of medical supplies and teams to European nations struggling to contain the pandemic.

Mr Trump and Mr Xi spoke just hours after the number of officially confirmed cases in the US exceeded those in China. The Chinese foreign ministry also announced late on Thursday that it would ban almost all foreign nationals from entering the country even if they held valid work and residential permits.

While the number of locally transmitted cases in China has dwindled over recent weeks, the government has been alarmed by a spike in so-called imported cases from people arriving in the world’s most populous nation. Most of the carriers, however, have been Chinese nationals.

China’s aviation regulator also said on Thursday that it would restrict all international airlines still operating flights to and from China to just one weekly service, in a move that will make it even more difficult for expatriate Chinese to return home.

Earlier on Thursday, Mr Trump and Mr Xi had both participated in an emergency videoconference of G20 leaders to discuss the pandemic.

The US has recorded 85,505 coronavirus cases with 1,288 deaths, compared to 81,340 and 3,292 respectively in China. But China’s official case numbers, unlike most other countries’, do not include “asymptomatic” carriers who do not exhibit any symptoms. If such cases were included, it is estimated that China’s official count could be as much as 50 per cent higher.

Before seeking reimbursement for services you can no longer use, it pays to know your consumer rights

Coronavirus disruption has changed our day-to-day lives beyond all recognition. Millions of households face difficult choices about their personal finances as they seek to rebalance their budgets and manage the cash flow crunch. 

Many will seek refunds on services they have committed to pay for, ranging from education to commuting costs and membership of gyms and clubs, which cannot be provided during the shutdown. Others are seeking refunds or insurance payouts on holidays and flights they had booked. 

In such unprecedented times, it pays to know your consumer rights, but these must be weighed against warnings from smaller businesses that failure to pay for services could result in their financial collapse. 

Private school fees

The final bell rang on Friday March 20, when the government announced it was closing schools to tackle the coronavirus pandemic. Experts say it is unlikely pupils will return before the end of the summer term and parents with children at fee-paying schools are asking whether they still have to pay. 

Some 615,000 children attend independent schools in the UK, with annual fees as high as £45,000 for boarding schools and £25,000 a year for some London day schools.

Under normal circumstances, the next payment date would be for the summer term due at the end of the Easter holidays in April. So will they be expected to pay? 

“This is a hugely difficult time for everyone,” says Julie Robinson, chief executive of the Independent Schools Council. “Schools are under immense pressures and this is one of the issues that will be dealt with at school level, depending on their individual policies and contracts with parents.

“We hope parents will bear with schools who need time to clarify government support measures and take stock of their situation and ongoing operations. They are focused on the welfare of their school communities and ensuring continuation of teaching and learning.

“Independent schools are fortunate to have access to effective online learning resources, enabling them to continue education remotely using technological solutions.”

Parents facing financial difficulties should contact their school as soon as possible, says Neil Roskilly, chief executive of the Independent Schools Association. All independent schools offer financial help to families, and while it is usually offered when a child enters a school, it can be extended to those families whose financial circumstances change.

Most private schools have funds available for this situation and can also defer fees if there is the prospect of future employment. This should be over a costed and reasonable timescale, usually is up to 12 months. Schools rarely charge interest.

To help bridge the gap between parental incomes and fees, more than £1bn a year is now provided in fee assistance to over 175,000 students, with about half allocated through means-testing.

“Schools are trying their best to maintain a ‘continuity of education’ via online technology and most parents we have spoken to understand that, and are choosing not to withhold fees,” says Mr Roskilly. “But in some cases, where schools have money in reserves, they are considering returning some of those fees to parents.”

Ellie Spencer, associate solicitor in the commercial dispute resolution team at law firm Goodman Derrick, says: “Parents are paying for a service and they might be able to argue that the school is not providing that service. Even if the school is providing online teaching, this is not the whole service, so parents might be entitled to a discount.”

Parents of children at private nurseries in the UK can pay about £1,000 a month for 50 hours a week for a child under two, but in London, the average Ofsted-rated facility charges between £70 and £85 a day.

Parents typically pay monthly for nurseries so most are receiving bills for April now when children are already at home. 

Nurseries are reacting to the closures in different ways. While some are charging full fees, others are offering discounts for all and some cutting costs specifically for families who have suffered a severe loss of income.

Nurseries have contracts with parents that are entered into when the child starts and the terms and conditions tend to require parents to give a month’s notice. They also usually require parents to continue paying fees during an emergency closure, but previously these have tended to be for a few days because of problems with the building. 

Purnima Tanuku, chief executive of National Day Nurseries Association, says: “Whether parents continue to pay fees when a closure is outside of a nursery’s control will depend on the agreements between individual nurseries and their parents. We’re pushing the government hard to offer sufficient financial support so nursery businesses can remain sustainable.”

One parent with two children under five at nursery contacted FT Money to say: “I've just received my monthly £2,000 bill with no offer of a discount. It seems that parents — many of whom can now not go to work — are expected to keep the nurseries going without receiving a service.” 

Lawyers say parents should negotiate. Edward Macey-Dare, a litigation and employment partner at Lee Bolton Monier-Williams, says: “Remember, nurseries are going to be under severe pressure as a result of the coronavirus situation and, if they play hardball, they are likely to face numerous parents giving notice to withdraw their children. It seems to me, therefore, that parents have the upper hand in this situation when it comes to negotiating a reduction in fees or more favourable payment terms.”

But others warn that without the financial support, private nurseries could collapse. “Some childminders and nurseries have asked parents to continue to pay their fees to retain their children’s places, even if they are not permitted to offer them childcare services,” says Lynne Rowland, a tax partner at Moore Kingston Smith.

“This is perhaps understandable in the absence of clarity over how the special financial measures apply. But the government should consider offering families full tax relief for these costs, which for many families are as essential as their mortgage or rent payments.”

The government has said that funding for early years entitlements covering up to 30 hours of childcare will continue during any periods of nursery closures. Some nurseries are encouraging key workers to continue sending their children into nursery so they can continue to access this government funding. 

For many commuters the cost of their annual season ticket is their second biggest monthly bill after their mortgage. To get the best deal, many pay upfront for the year, possibly with an interest-free loan from their employers.

Train companies say annual season tickets will be refunded pro-rata, but to get any money back commuters must have 12 weeks remaining on them. This is because they effectively get 12 weeks of free travel on an annual season ticket. Monthly season tickets need at least six days remaining and weekly ones at least two days. The £10 administrative fee will be waived.

Someone who bought an annual season ticket for £4,980 at the beginning of the year should be able to get a refund for six months’ travel or £2,490. Refunds should be paid within 28 days. Full refunds can also be claimed for advance and off-peak tickets booked but not used — apply via train company websites. 

Transport for London is slightly more generous. It requires six weeks to remain on annual season tickets, seven days on a monthly ticket and three days on a seven-day ticket, and does not charge an administrative fee. Apply for a refund via its website. 

Many commuters pay to guarantee a place in their station car park by buying an annual season ticket. A typical permit costs over £1,000. Apply online for refunds to the company that runs the car park. 

With no live football likely until June at the earliest and many other major sporting events cancelled or postponed, subscribers to Sky Sports can pause their sports subscription online and it will automatically resume when live football and other major sporting events return. 

A message on Sky’s website reads: “While we expect that many of the recently postponed sports events will eventually go ahead, if you wish to pause your sports subscription in the meantime you will not be charged a fee to do so or be held to any notice period.”

BT Sport says that customers on its new “flexible TV” package can pause their subscription and make other changes by logging on to bt.com/tv.

BT says: “For now, we have been busy working on a revised schedule for BT Sport which will include variations of popular shows such as Premier League Tonight, live WWE, Rugby Tonight, BT Sport Films and ESPN Films, recent boxing events and classic football, rugby and other sport fixtures from across the years.

 

“We understand that this is a difficult time for customers and if they wish to discuss their BT Sport contract or other options, would ask they give us a call.”

When it comes to live sporting events, season ticket holders should check the terms and conditions of their clubs. Tickets for postponed games are usually valid when the game is finally played.

For example, Arsenal’s terms and conditions read: “The club reserves the right to reschedule any match or, if necessary, play the match out of view of the public, without notice and without any liability whatsoever.”

Manchester United’s say: “Where any match is cancelled, abandoned or postponed the club shall have no liability whatsoever to ticket holders,” although ticket holders would be entitled to attend rearranged matches.

People who had secured Glastonbury tickets have been told that their £50 deposits will be rolled over to next year, after this year’s festival was cancelled.

People with tickets for shows and gigs that have been postponed may find they can only get refunds if they cannot attend the new date. For example, tickets for Trevor Noah at the O2 centre at the beginning of April can be used at the rescheduled shows in September.

Gym members who may have found it difficult to end membership contracts in the past could find that their fees stop automatically.

Virgin Active is automatically freezing all memberships at its clubs with no fees to pay until they reopen. It is crediting members with any fees that have already been paid for April and will also credit for March 21 to 31. Its social channels @VirginActiveUK remain open with advice on workouts to do at home.

Gymbox says that for as long as its clubs are closed there will be a freeze on monthly memberships. No payments will be taken for April and any future months it is closed, and fees for time lost in March will also be credited.

Competition in the gym market means many clubs charge on a month-to-month basis, but fixed memberships could prove trickier to cancel — check the terms of your contract to see if a percentage of your fees could be refunded. 

Gym members who may have found it difficult to end membership contracts in the past could find that their fees stop automatically.

Virgin Active is automatically freezing all memberships at its clubs with no fees to pay until they reopen. It is crediting members with any fees that have already been paid for April and will also credit for March 21 to 31. Its social channels @VirginActiveUK remain open with advice on workouts to do at home.

Gymbox says that for as long as its clubs are closed there will be a freeze on monthly memberships. No payments will be taken for April and any future months it is closed, and fees for time lost in March will also be credited.

Competition in the gym market means many clubs charge on a month-to-month basis, but fixed memberships could prove trickier to cancel — check the terms of your contract to see if a percentage of your fees could be refunded. 

If your flight or package holiday was scheduled before April 16 and is cancelled, you do not have to accept a voucher or credit note or be forced to rebook. You are legally entitled to a refund.

The advice not to travel abroad from the Foreign and Commonwealth Office (FCO) also means you should be able to claim from your travel insurer for consequential losses, such as booked hotel rooms or car hire.

When flights and holidays are cancelled, airlines and travel agents are obliged to issue refunds or allow you to rebook for a future date. Under the Package Holiday and Linked Travel Regulations 2018, holidaymakers are also due a full refund.

However, consumer group Which? has found that many companies are ignoring this requirement and are only offering consumers credit vouchers or the chance to reschedule.

Martyn James of Resolver, a free online complaints company, says: “If the hotel, holiday pr flight has been cancelled then you should get a refund as it’s not you, it’s them.”

If firms insist on providing vouchers instead of refunding, he says: “Ask the firm to send you the terms and conditions where it says they can do this. If you don’t think it’s fair, make a complaint.”

British Airways says it will rebook or refund for tickets under its “Manage My Booking” facility. Ryanair has removed its flight change fees on all bookings next month.

Airlines are experiencing an extremely high volume of calls. BA, easyJet, Ryanair and Virgin Atlantic are asking that only passengers who were due to travel in the next 72 hours call or message, so they can help those needing urgent rebooking.

Most travel insurers will ask you to seek a refund from the travel firm first, but if your policy covers you for cancellation, then you can make a claim.

Airbnb says that reservations for stays and experiences made on or before March 14 with a check-in date between then and April 14 will be eligible for a full refund. If a hotel has closed, you are also due a full refund.

If airlines or holiday companies will not pay for cancelled flights or holidays, those who paid by credit card should be able to get compensation under Section 75 of the Consumer Credit Act. But if the hotel is still able to offer the accommodation you are unlikely to get a refund because the provider has not broken their agreement with you.

For bookings after April 16, the situation is less clear. Holidaymakers will have to wait to find out if their flights are affected and what the FCO advice is on travel at that time.