'How Remdesivir, New Hope for Covid-19 Patients, Was Resurrected' diff viewer (18/19)

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How Remdesivir, New Hope for Covid-19 Patients, Was Resurrected	How Remdesivir, New Hope for Covid-19 Patients, Was Resurrected
2020-07-03 00:52:55 UTC	2020-07-17 06:26:27 UTC (14 days later)
Remdesivir, an antiviral drug designed to treat both hepatitis and a common respiratory virus, seemed fated to join thousands of other failed medications after proving useless against those diseases. The drug was consigned to the pharmaceutical scrap heap, all but forgotten by the scientists who once championed it.	Remdesivir, an antiviral drug designed to treat both hepatitis and a common respiratory virus, seemed fated to join thousands of other failed medications after proving useless against those diseases. The drug was consigned to the pharmaceutical scrap heap, all but forgotten by the scientists who once championed it.
But on Friday, the Food and Drug Administration issued an emergency approval for remdesivir as a treatment for patients severely ill with Covid-19, the disease caused by the coronavirus.	But on Friday, the Food and Drug Administration issued an emergency approval for remdesivir as a treatment for patients severely ill with Covid-19, the disease caused by the coronavirus.
The story of remdesivir’s rescue and transformation testifies to the powerful role played by federal funding, which allowed scientists laboring in obscurity to pursue basic research without obvious financial benefits. This research depends almost entirely on government grants.	The story of remdesivir’s rescue and transformation testifies to the powerful role played by federal funding, which allowed scientists laboring in obscurity to pursue basic research without obvious financial benefits. This research depends almost entirely on government grants.
Dr. Mark Denison of Vanderbilt University is one of a handful of researchers who discovered remdesivir’s potential. He began studying coronaviruses a quarter-century ago, a time when few scientists cared about them — the ones infecting humans caused colds, he recalled, and scientists just wanted to know how they worked.	Dr. Mark Denison of Vanderbilt University is one of a handful of researchers who discovered remdesivir’s potential. He began studying coronaviruses a quarter-century ago, a time when few scientists cared about them — the ones infecting humans caused colds, he recalled, and scientists just wanted to know how they worked.
“We were interested from the biologic perspective,” Dr. Denison recalled. “No one was interested from a therapeutic perspective.”	“We were interested from the biologic perspective,” Dr. Denison recalled. “No one was interested from a therapeutic perspective.”
Neither he nor the scores of other scientists interested in coronaviruses foresaw that a new one would unleash a plague that has killed nearly a quarter-million people worldwide. The F.D.A. rushed to approve remdesivir under emergency use provisions, after a federal trial demonstrated modest improvements in severely ill patients.	Neither he nor the scores of other scientists interested in coronaviruses foresaw that a new one would unleash a plague that has killed nearly a quarter-million people worldwide. The F.D.A. rushed to approve remdesivir under emergency use provisions, after a federal trial demonstrated modest improvements in severely ill patients.
The trial, sponsored by the National Institute of Allergy and Infectious Diseases, included more than 1,000 hospitalized patients and found that those receiving remdesivir recovered faster than those who got a placebo: in 11 days, versus 15 days.	The trial, sponsored by the National Institute of Allergy and Infectious Diseases, included more than 1,000 hospitalized patients and found that those receiving remdesivir recovered faster than those who got a placebo: in 11 days, versus 15 days.
But the drug did not significantly reduce fatality rates, and some critics noted that the trial’s primary endpoint — its measure of success — had been greatly simplified to emphasize time to recovery.	But the drug did not significantly reduce fatality rates, and some critics noted that the trial’s primary endpoint — its measure of success — had been greatly simplified to emphasize time to recovery.
A half-dozen experts contacted by The Times on Thursday said the change was necessary. Officials at N.I.A.I.D. said biostatisticians urging the revision had not seen the data and were not aiming for a particular result.	A half-dozen experts contacted by The Times on Thursday said the change was necessary. Officials at N.I.A.I.D. said biostatisticians urging the revision had not seen the data and were not aiming for a particular result.
Dr. Anthony S. Fauci, director of the institute, said the results were “a very important proof of concept” but not a “knockout.” President Trump hailed the drug on Friday as “an important treatment” and “really promising.”	Dr. Anthony S. Fauci, director of the institute, said the results were “a very important proof of concept” but not a “knockout.” President Trump hailed the drug on Friday as “an important treatment” and “really promising.”
Remdesivir is approved only for severely ill patients and only temporarily; formal approval must come later. Still, some doctors laboring in intensive care units embraced the drug as an important new weapon against a virus that is killing patients worldwide.	Remdesivir is approved only for severely ill patients and only temporarily; formal approval must come later. Still, some doctors laboring in intensive care units embraced the drug as an important new weapon against a virus that is killing patients worldwide.
“It’s a great first step,” said Dr. Robert Finberg, chairman of the department of medicine at the University of Massachusetts Medical School.	“It’s a great first step,” said Dr. Robert Finberg, chairman of the department of medicine at the University of Massachusetts Medical School.
Little about the early history of remdesivir, manufactured by Gilead Sciences, suggested the hopes now placed upon it.	Little about the early history of remdesivir, manufactured by Gilead Sciences, suggested the hopes now placed upon it.
Coronaviruses hold much more RNA than scientists once theorized a virus could. Many viruses that cause epidemics rely on this type of genetic material, and almost all mutate constantly. That is why flu viruses change from year to year.	Coronaviruses hold much more RNA than scientists once theorized a virus could. Many viruses that cause epidemics rely on this type of genetic material, and almost all mutate constantly. That is why flu viruses change from year to year.
Yet coronaviruses did not change much — their mutation rate is about one-twentieth the rate of other RNA viruses.	Yet coronaviruses did not change much — their mutation rate is about one-twentieth the rate of other RNA viruses.
In 2007, Dr. Denison discovered that coronaviruses have a powerful “proofreading” system. If an error occurs in copying RNA as the coronavirus replicates, it corrects the error. In lab experiments, coronaviruses that mutated were weaker, outcompeted by those without mutations.	In 2007, Dr. Denison discovered that coronaviruses have a powerful “proofreading” system. If an error occurs in copying RNA as the coronavirus replicates, it corrects the error. In lab experiments, coronaviruses that mutated were weaker, outcompeted by those without mutations.
Dr. Denison and other experts wondered if it might be possible to trick the virus with a drug that dodged the proofreading system and blocked the virus’s growing RNA chain, making it prematurely terminate.	Dr. Denison and other experts wondered if it might be possible to trick the virus with a drug that dodged the proofreading system and blocked the virus’s growing RNA chain, making it prematurely terminate.
Talking about this problem with another scientist at a meeting, Dr. Denison learned that Gilead Sciences had dozens of drugs that might do the trick. “All of these compounds had been shelved for one reason or another,” Dr. Denison said.	Talking about this problem with another scientist at a meeting, Dr. Denison learned that Gilead Sciences had dozens of drugs that might do the trick. “All of these compounds had been shelved for one reason or another,” Dr. Denison said.
Most worked in lab tests to shut down coronaviruses, he found — some better than others. One of the best was GS-5734, now known as remdesivir. “I like to call it the Terminator,” Dr. Denison said.	Most worked in lab tests to shut down coronaviruses, he found — some better than others. One of the best was GS-5734, now known as remdesivir. “I like to call it the Terminator,” Dr. Denison said.
Dr. Denison discovered remdesivir was just what they were seeking: a drug that slipped past the viruses’ powerful system to protect RNA, their genetic material. Remdesivir made growing chains of the viral RNA terminate prematurely, killing the virus.	Dr. Denison discovered remdesivir was just what they were seeking: a drug that slipped past the viruses’ powerful system to protect RNA, their genetic material. Remdesivir made growing chains of the viral RNA terminate prematurely, killing the virus.
Remdesivir killed every known coronavirus in Dr. Denison’s tests. Then researchers at the University of North Carolina found that the drug also killed the viruses in infected animals.	Remdesivir killed every known coronavirus in Dr. Denison’s tests. Then researchers at the University of North Carolina found that the drug also killed the viruses in infected animals.
	Updated July 7, 2020
	The coronavirus can stay aloft for hours in tiny droplets in stagnant air, infecting people as they inhale, mounting scientific evidence suggests. This risk is highest in crowded indoor spaces with poor ventilation, and may help explain super-spreading events reported in meatpacking plants, churches and restaurants. It’s unclear how often the virus is spread via these tiny droplets, or aerosols, compared with larger droplets that are expelled when a sick person coughs or sneezes, or transmitted through contact with contaminated surfaces, said Linsey Marr, an aerosol expert at Virginia Tech. Aerosols are released even when a person without symptoms exhales, talks or sings, according to Dr. Marr and more than 200 other experts, who have outlined the evidence in an open letter to the World Health Organization.
	Common symptoms include fever, a dry cough, fatigue and difficulty breathing or shortness of breath. Some of these symptoms overlap with those of the flu, making detection difficult, but runny noses and stuffy sinuses are less common. The C.D.C. has also added chills, muscle pain, sore throat, headache and a new loss of the sense of taste or smell as symptoms to look out for. Most people fall ill five to seven days after exposure, but symptoms may appear in as few as two days or as many as 14 days.
	Scientists around the country have tried to identify everyday materials that do a good job of filtering microscopic particles. In recent tests, HEPA furnace filters scored high, as did vacuum cleaner bags, fabric similar to flannel pajamas and those of 600-count pillowcases. Other materials tested included layered coffee filters and scarves and bandannas. These scored lower, but still captured a small percentage of particles.
	A commentary published this month on the website of the British Journal of Sports Medicine points out that covering your face during exercise “comes with issues of potential breathing restriction and discomfort” and requires “balancing benefits versus possible adverse events.” Masks do alter exercise, says Cedric X. Bryant, the president and chief science officer of the American Council on Exercise, a nonprofit organization that funds exercise research and certifies fitness professionals. “In my personal experience,” he says, “heart rates are higher at the same relative intensity when you wear a mask.” Some people also could experience lightheadedness during familiar workouts while masked, says Len Kravitz, a professor of exercise science at the University of New Mexico.
	The steroid, dexamethasone, is the first treatment shown to reduce mortality in severely ill patients, according to scientists in Britain. The drug appears to reduce inflammation caused by the immune system, protecting the tissues. In the study, dexamethasone reduced deaths of patients on ventilators by one-third, and deaths of patients on oxygen by one-fifth.
	The coronavirus emergency relief package gives many American workers paid leave if they need to take time off because of the virus. It gives qualified workers two weeks of paid sick leave if they are ill, quarantined or seeking diagnosis or preventive care for coronavirus, or if they are caring for sick family members. It gives 12 weeks of paid leave to people caring for children whose schools are closed or whose child care provider is unavailable because of the coronavirus. It is the first time the United States has had widespread federally mandated paid leave, and includes people who don’t typically get such benefits, like part-time and gig economy workers. But the measure excludes at least half of private-sector workers, including those at the country’s largest employers, and gives small employers significant leeway to deny leave.
	So far, the evidence seems to show it does. A widely cited paper published in April suggests that people are most infectious about two days before the onset of coronavirus symptoms and estimated that 44 percent of new infections were a result of transmission from people who were not yet showing symptoms. Recently, a top expert at the World Health Organization stated that transmission of the coronavirus by people who did not have symptoms was “very rare,” but she later walked back that statement.
	Touching contaminated objects and then infecting ourselves with the germs is not typically how the virus spreads. But it can happen. A number of studies of flu, rhinovirus, coronavirus and other microbes have shown that respiratory illnesses, including the new coronavirus, can spread by touching contaminated surfaces, particularly in places like day care centers, offices and hospitals. But a long chain of events has to happen for the disease to spread that way. The best way to protect yourself from coronavirus — whether it’s surface transmission or close human contact — is still social distancing, washing your hands, not touching your face and wearing masks.
	A study by European scientists is the first to document a strong statistical link between genetic variations and Covid-19, the illness caused by the coronavirus. Having Type A blood was linked to a 50 percent increase in the likelihood that a patient would need to get oxygen or to go on a ventilator, according to the new study.
	If air travel is unavoidable, there are some steps you can take to protect yourself. Most important: Wash your hands often, and stop touching your face. If possible, choose a window seat. A study from Emory University found that during flu season, the safest place to sit on a plane is by a window, as people sitting in window seats had less contact with potentially sick people. Disinfect hard surfaces. When you get to your seat and your hands are clean, use disinfecting wipes to clean the hard surfaces at your seat like the head and arm rest, the seatbelt buckle, the remote, screen, seat back pocket and the tray table. If the seat is hard and nonporous or leather or pleather, you can wipe that down, too. (Using wipes on upholstered seats could lead to a wet seat and spreading of germs rather than killing them.)
	If you’ve been exposed to the coronavirus or think you have, and have a fever or symptoms like a cough or difficulty breathing, call a doctor. They should give you advice on whether you should be tested, how to get tested, and how to seek medical treatment without potentially infecting or exposing others.
That included not just coronaviruses that cause the common cold, but also SARS and MERS — even a coronavirus that infects only mice.	That included not just coronaviruses that cause the common cold, but also SARS and MERS — even a coronavirus that infects only mice.
But the drug failed a number of real-life tests, not just against hepatitis but also against Ebola in Africa. The drug languished, unapproved for any use — until a new coronavirus emerged.	But the drug failed a number of real-life tests, not just against hepatitis but also against Ebola in Africa. The drug languished, unapproved for any use — until a new coronavirus emerged.
As SARS-CoV-2, the virus that causes Covid-19, began to grow into a pandemic, many scientists realized that remdesivir might be the best solution at hand. It had already undergone animal testing and safety testing in humans.	As SARS-CoV-2, the virus that causes Covid-19, began to grow into a pandemic, many scientists realized that remdesivir might be the best solution at hand. It had already undergone animal testing and safety testing in humans.
So doctors began giving it to patients in studies without controls and even outside of studies altogether. Anecdotes fueled demand. Gilead sponsored some of these studies and gave the drug to doctors who treated hundreds of patients under compassionate use, a legal exemption permitting use of an unapproved drug to treat patients.	So doctors began giving it to patients in studies without controls and even outside of studies altogether. Anecdotes fueled demand. Gilead sponsored some of these studies and gave the drug to doctors who treated hundreds of patients under compassionate use, a legal exemption permitting use of an unapproved drug to treat patients.
But none of this could demonstrate that a drug was helpful to patients. It took the federal trial, in which many patients were given a placebo, to show that remdesivir seems to have a modest effect.	But none of this could demonstrate that a drug was helpful to patients. It took the federal trial, in which many patients were given a placebo, to show that remdesivir seems to have a modest effect.