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Javier E

Most New York Coronavirus Cases Came From Europe, Genomes Show - The New York Times - 0 views

  • New research indicates that the coronavirus began to circulate in the New York area by mid-February, weeks before the first confirmed case, and that travelers brought in the virus mainly from Europe, not Asia.
  • The research revealed a previously hidden spread of the virus that might have been detected if aggressive testing programs had been put in place.
  • It would not be until late February that Italy would begin locking down towns and cities, and March 11 when Mr. Trump said he would block travelers from most European countries. But New Yorkers had already been traveling home with the virus.
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  • While conspiracy theories might falsely claim the virus was concocted in a lab, the virus’s genome makes clear that it arose in bats.
  • Sophisticated computer programs can then figure out how all of those mutations arose as viruses descended from a common ancestor. If they get enough data, they can make rough estimates about how long ago those ancestors lived. That’s because mutations arise at a roughly regular pace, like a molecular clock.
  • Tracking viral mutations demands sequencing all the genetic material in a virus — its genome. Once researchers have gathered the genomes from a number of virus samples, they can compare their mutations.
  • In January, a team of Chinese and Australian researchers published the first genome of the new virus. Since then, researchers around the world have sequenced over 3,000 more. Some are genetically identical to each other, while others carry distinctive mutations.
  • The most closely related coronavirus is in a Chinese horseshoe bat, the researchers found. But the new virus has gained some unique mutations since splitting off from that bat virus decades ago.
  • Dr. Boni said that ancestral virus probably gave rise to a number of strains that infected horseshoe bats, and perhaps sometimes other animals.
  • It’s entirely possible, Dr. Boni said, in the past 10 or 20 years, a hybrid virus arose in some horseshoe bat that was well-suited to infect humans, too. Later, that virus somehow managed to cross the species barrier.
  • already, the genomes of the virus are revealing previously hidden outlines of its history over the past few months.
  • While the coronavirus mutations are useful for telling lineages apart, they don’t have any apparent effect on how the virus works.
  • The deepest branches of the tree all belong to lineages from China. The Nextstrain team has also used the mutation rate to determine that the virus probably first moved into humans from an animal host in late 2019.
  • In January, as the scope of the catastrophe in China became clear, a few countries started an aggressive testing program. They were able to track the arrival of the virus on their territory and track its spread through their populations.
  • But the United States fumbled in making its first diagnostic kits and initially limited testing only to people who had come from China and displayed symptoms of Covid-19.“It was a disaster that we didn’t do testing,”
  • As new cases arose in other parts of the country, other researchers set up their own pipelines. The first positive test result in New York came on March 1, and after a couple of weeks, patients surged into the city’s hospitals.
  • Dr. Heguy and her colleagues found some New York viruses that shared unique mutations not found elsewhere. “That’s when you know you’ve had a silent transmission for a while,”
  • And researchers at Mount Sinai started sequencing the genomes of patients coming through their hospital. They found that the earliest cases identified in New York were not linked to later ones.“Two weeks later, we start seeing viruses related to each other,”
  • Dr. Gonzalez-Reiche and her colleagues found that these viruses were practically identical to viruses found around Europe.
  • hey write that the viruses reveal “a period of untracked global transmission between late January to mid-February.”
  • Dr. van Bakel and his colleagues found one New York virus that was identical to one of the Washington viruses found by Dr. Bedford and his colleagues. In a separate study, researchers at Yale found another Washington-related virus. Combined, the two studies hint that the coronavirus has been moving from coast to coast for several weeks.
  • Dr. Boni and his colleagues found that the genome of the new virus contains a number of mutations in common with strains of coronaviruses that infect bats.
  • Some viruses evolve so quickly that they require vaccines that can produce several different antibodies. That’s not the case for Covid-19. Like other coronaviruses, it has a relatively slow mutation rate compared to some viruses, like influenza.
Javier E

As Coronavirus Mutates, the World Stumbles Again to Respond - The New York Times - 0 views

  • Denmark, which has invested in genetic surveillance, discovered the variant afflicting Britain in multiple Danish regions and recently tightened restrictions. The health minister compared it to a storm surge, predicting that it would dominate other variants by mid-February.
  • And as countries go looking, they are discovering other variants, too.
  • With the world stumbling in its vaccination rollout and the number of cases steeply rising to peaks that exceed those seen last spring, scientists see a pressing need to immunize as many people as possible before the virus evolves enough to render the vaccines impotent.
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  • “We do know how to dial down the transmission of the virus by a lot with our behavior,” said Carl T. Bergstrom, an evolutionary biologist at the University of Washington in Seattle. “We’ve got a lot of agency there.”
  • The vaccine alone will not be enough to get ahead of the virus: It will take years to inoculate enough people to limit its evolution. In the meantime, social distancing, mask-wearing and hand-washing — coupled with aggressive testing, tracking and tracing — might buy some time and avert devastating spikes in hospitalizations and deaths along the way. These strategies could still turn the tide against the virus, experts said.
  • “It’s a race against time,” said Marion Koopmans, a Dutch virologist and a member of a World Health Organization working group on coronavirus adaptations.
  • experts had warned from the start that it would only be a matter of time before the virus became an even more formidable adversary.
  • The spread of the variant lashing Britain has left some countries vulnerable at a time when they seemed on the brink of scientific salvation.A case in point: Israel. The country, which had launched a remarkably successful vaccine rollout, tightened its lockdown on Friday after having discovered cases of the variant. About 8,000 new infections have been detected daily in recent days, and the rate of spread in ultra-Orthodox communities has increased drastically.
  • Yet in the course of the pandemic, governments have often proven reluctant or unable to galvanize support for those basic defenses. Many countries have all but given up on tracking and tracing. Mask-wearing remains politically charged in the United States, despite clear evidence of its efficacy.
  • “Every situation we have studied in depth, where a virus has jumped into a new species, it has become more contagious over time,” said Andrew Read, an evolutionary microbiologist at Penn State University. “It evolves because of natural selection to get better, and that’s what’s happening here.”
  • Experts say that countries should focus instead on ramping up vaccinations, particularly among essential workers who face a high risk with few resources to protect themselves. The longer the virus spreads among the unvaccinated, the more mutations it might collect that can undercut the vaccines’ effectiveness.
  • The variants that have emerged in South Africa and Brazil are a particular threat to immunization efforts, because both contain a mutation associated with a drop in the efficacy of vaccines. In one experiment, designed to identify the worst-case scenario, Dr. Bloom’s team analyzed 4,000 mutations, looking for those that would render vaccines useless. The mutation present in the variants from both Brazil and South Africa proved to have the biggest impact.
  • Still, every sample of serum in the study neutralized the virus, regardless of its mutations, Dr. Bloom said, adding that it would take a few more years before the vaccines need to be tweaked.“There should be plenty of time where we can be prospective, identify these mutations, and probably update the vaccines in time.”
  • Dr. Rambaut and colleagues released a paper on the variant discovered in Britain on Dec. 19 — the same day that British officials announced new measures. The variant had apparently been circulating undetected as early as September. Dr. Rambaut has since credited the South Africa team with the tip that led to the discovery of the variant surging in Britain.
  • Public health officials have formally recommended that type of swift genetic surveillance and information-sharing as one of the keys to staying on top of the ever-changing virus. But they have been calling for such routine surveillance for years, with mixed results.
  • Britain has one of the most aggressive surveillance regimens, analyzing up to 10 percent of samples that test positive for the virus. But few countries have such robust systems in place. The United States sequences less than 1 percent of its positive samples. And others cannot hope to afford the equipment or build such networks in time for this pandemic.
anonymous

Early Coronavirus Mutation Made It Harder to Stop, Evidence Suggests - The New York Times - 0 views

  • one mutation near the beginning of the pandemic did make a difference, multiple new findings suggest, helping the virus spread more easily from person to person and making the pandemic harder to stop.
  • The mutation, known as 614G, was first spotted in eastern China in January and then spread quickly throughout Europe and New York City.
  • Researchers at Los Alamos National Laboratory argued in May that the variant had probably evolved the ability to infect people more efficiently.
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  • But a host of new research — including close genetic analysis of outbreaks and lab work with hamsters and human lung tissue — has supported the view that the mutated virus did in fact have a distinct advantage
  • There is no evidence that a coronavirus with the 614G mutation causes more severe symptoms, kills more people or complicates the development of vaccines.
  • But other researchers said that a lack of proper containment measures, not the mutation, is largely to blame for resurgent outbreaks.
  • The original variant spotted in Wuhan, China, in late 2019 was already highly contagious
  • Even so, Dr. Andersen said that the variant’s higher transmissibility could help explain why some countries that were initially successful in containing the virus became susceptible to it later. The virus may have been “harder to contain than the first time around,” he said.
  • But the subtle change in the virus’ genome appears to have had a big ripple effect
  • Scientists consider animal experiments a critical step to test whether a mutation that makes viruses more infectious in a lab dish also does so in a living population.
  • The virus will continue to change. and while most of those changes will be mere typos, some may be more meaningful, Dr. Engelthaler said. “There will be the possibility of additional alterations that change the nature of the pandemic,” he said.
Javier E

Health Experts Warily Eye XBB.1.5, the Latest Omicron Subvariant - The New York Times - 0 views

  • Most recombinant SARS-CoV-2 viruses have dwindled away in a matter of weeks or months, unable to outcompete other lineages. XBB, on the other hand, got a winning ticket in the genetic lottery.
  • From one parent, it gained a set of mutations that helped it evade antibodies from previous infections and vaccinations. From the other parent, it gained a separate set of mutations that made it even more evasive.
  • “XBB literally picked up the most possible mutations that it could possibly pick up from those two parents,” said Thomas Peacock, a virologist at Imperial College London. The new combination made XBB one of the most evasive Omicron subvariants in existence last summer.
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  • Recent experiments suggest that XBB paid a steep price for its power to evade immunity. The mutations allow it to escape antibodies by altering the shape of the protein, called spike, that covers its surface. But some of those mutations also make it harder for XBB spike proteins to grab tightly to cells — the first step required for an infection.
  • That loose grip may have lessened XBB’s advantage against other forms of the virus. In late 2022, it jostled alongside a number of other Omicron subvariants. In Singapore, XBB caused a surge in October, for example, while remaining rare in many other parts of the world.
  • As XBB multiplied, it continued to mutate into new forms. The earliest samples of XBB.1.5 were isolated in October in New York. The new subvariant gained one crucial mutation, known as F486P.
  • Yunlong Cao of Peking University and his colleagues tested out XBB.1.5 in dishes of cells, comparing how it fared against earlier forms of XBB. The researchers found that the F486P mutation allowed XBB.1.5 to grab tightly to cells again. But the new subvariant could still evade antibodies as well as earlier forms of XBB.
  • In Connecticut, for example, Nathan Grubaugh at Yale University and his colleagues found that by mid-December, other Omicron subvariants were falling. Only XBB.1.5 cases were growing. Dr. Grubaugh estimates that it is about 20 percent more transmissible than BQ.1, which had been the dominant form.
  • How severe XBB.1.5 infections are compared with other forms of the coronavirus is not yet clear. “It’s serious,” Dr. Grubaugh said. “I just don’t necessarily know if it’s really more serious than some of the other Omicron lineages in terms of the overall impact.”
  • XBB.1.5 has already spread to other countries, and is growing rapidly in Germany, Denmark and elsewhere in Europe
  • Scientists are already scanning new sequences being uploaded to an international database called GISAID in the hopes of spotting an upgraded version of XBB.1.5. But their job is getting harder because governments are pulling back on sequencing efforts. “Worldwide, sequencing has taken a real hit,” Dr. Peacock said.
  • The United States, which once lagged behind other nations, has managed to maintain a fairly strong sequencing effort. Without it, Dr. Peacock said, XBB.1.5 might have stayed below the radar for much longer. If XBB.1.5’s next generation is evolving somewhere with little sequencing, it may go undetected for some time to come.
  • Dr. Lemieux said that paring back on sequencing was a mistake, given how many infections and deaths the virus is still causing. “This is a part of public health,” he said.
Javier E

In Iceland's DNA, New Clues to Disease-Causing Genes - NYTimes.com - 0 views

  • Scientists in Iceland have produced an unprecedented snapshot of a nation’s genetic makeup, discovering a host of previously unknown gene mutations that may play roles in ailments as diverse as Alzheimer’s disease, heart disease and gallstones.
  • Decode, an Icelandic genetics firm owned by Amgen, described sequencing the genomes — the complete DNA — of 2,636 Icelanders, the largest collection ever analyzed in a single human population.
  • With this trove of genetic information, the scientists were able to accurately infer the genomes of more than 100,000 other Icelanders, or almost a third of the entire country
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  • While some diseases, like cystic fibrosis, are caused by a single genetic mutation, the most common ones are not. Instead, mutations to a number of different genes can each raise the risk of getting, say, heart disease or breast cancer. Discovering these mutations can shed light on these diseases and point to potential treatments. But many of them are rare, making it necessary to search large groups of people to find them.
  • The wealth of data created in Iceland may enable scientists to begin doing that
  • For example, they found eight people in Iceland who shared a mutation on a gene called MYL4. Medical records showed that they also have early onset atrial fibrillation, a type of irregular heartbeat.
  • they identified a gene called ABCA7 as a risk factor for Alzheimer’s disease.Previous studies had suggested a gene in the genetic neighborhood of ABCA7 was associated with the disease.But the Icelandic study pinpointed the gene itself — and even the specific mutation involved.
  • Since Dr. Stefansson and his colleagues submitted their initial results for publication, they have continued gathering DNA from Icelanders.The scientists now have full genomes from about 10,000 Icelanders and partial genetic information on 150,000 more.
  • Dr. Stefansson said that means that his firm could generate a report for genetic disease on every person in Iceland
  • Iceland is a particularly fertile country for doing genetics research. It was founded by a small number of settlers from Europe arriving about 1,100 years ago. Between 8,000 and 20,000 people came mainly from Scandinavia, Ireland and Scotland.
  • The country remained isolated for the next thousand years, and so living Icelanders have a relatively low level of genetic diversity. This makes it easier for scientists to detect genetic variants that raise the risk of disease, because there are fewer of them to examine.
  • celand also has impressive genealogical records. Through epic poems and historical documents, many Icelanders can trace their ancestry back to the nation’s earliest arrivals. Geneticists use national genealogy databases to look for diseases that are unusually common in relatives — a sign that they share a mutation.
  • the company is now investigating a gene, found by Decode, with a strong link to cardiovascular disease in Iceland. (He declined to name the gene.)
yehbru

Why The Coronavirus Variant From Brazil Is Especially Worrisome To Scientists : Goats a... - 0 views

  • There's one from the U.K., which is more contagious and already circulating in the United States. There's one from South Africa, which is forcing Moderna and Pfizer to reformulate their COVID-19 vaccines and create "booster" shots, just to make sure the vaccines maintain their efficacies.
  • A variant called P.1, which emerged in early December in Manaus, Brazil, and by mid-January had already caused a massive resurgence in cases across the city of 2 million people.
  • "Manaus already had 75% of people infected [in the spring of last year]."
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  • Scientists don't understand why the variant has spread so explosively in Brazil, and the variant carries a particularly dangerous set of mutations.
  • One study estimated that the population should have reached herd immunity and the virus shouldn't be able to spread easily in the community. So why would the city see an even bigger surge 10 months later? Could P.1 be evading the antibodies made against the previous version of the virus, making reinfections easier?
  • "So when we see a whole lot of mutations in [those surfaces], it raises the possibility that the mutations might be conferring immune escape." That is, the mutations are helping the virus evade antibodies or escape recognition by them. In essence, the mutations are providing the virus with a type of invisibility cloak.
  • "In fact, it was really quite a dramatic drop-off in sensitivity. We saw that in half of the serum, the antibodies were significantly less effective against the new variant [from South Africa]." So far, scientists haven't tested out P.1 in similar neutralization experiments, but P.1 has two mutations that scientists have already shown reduce antibody binding.
  • "We've been here before with the flu. We're having to live with influenza and figure out a way of staying ahead of the virus by making vaccines on a yearly basis," said Gupta at the University of Cambridge.
Javier E

The Coronavirus Brazil Variant Shows the World's Vulnerability - The Atlantic - 0 views

  • Though many questions remain, one plausible explanation is that people who have already been infected by the virus are getting sick—and not mildly so. That possibility has been long feared throughout the pandemic, yet not previously seen on any significant scale
  • Although no known variants have been found to pose an immediate threat to vaccinated people, the capacity for reinfection to any significant degree would reshape the pandemic’s trajectory.
  • The new wave of COVID-19 cases in Manaus occurred about eight months after the initial wave. People might have lost some degree of immunity during that window.
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  • Two important factors seem to be playing a role in Brazil’s resurgence. The first is that, after a COVID-19 infection, the natural immunity that our bodies develop seems to vary in strength and permanence. Protection wanes after infection with most respiratory viruses, including coronaviruses
  • The solution, then, depends on vaccination. The immune response that the vaccines create is generally more robust than the immune response we get after being infected by a virus, and should buy a population more protected time than would a surge in exposure to the virus
  • it at least has a capacity to infect people who have already recovered from COVID-19, even if their defenses protect them against other versions of the virus.
  • The mutations that help the virus spread and evade immune responses have arisen independently in multiple places. Combined with waning immunity, these factors underscore the challenge before the world: Populations may still be vulnerable to disaster scenarios just when things seem to be getting better.
  • the virus’s capacity to cause such a deadly second surge in Brazil suggests a dangerous evolutionary potential.
  • New, dangerous variants are all but inevitable when there are extremely high levels of transmission of the virus. As more people gain immunity, the selective pressure on the virus will favor the variants that can most effectively evade immune responses
  • the basic nature of evolutionary biology means that the virus should be expected to evolve in ways that circumvent defense mechanisms. Evidence that it is already doing so has been clear in the latest vaccine trial data.
  • the variant in Brazil, known as the P.1 (or B.1.1.248) lineage, has a potent combination of mutations. Not only does this variant seem to be more transmissible; its lineage carries mutations that help it escape the antibodies that we develop in response to older lineages of the coronavirus.
  • Wealthy countries have time to avoid a fate like Brazil’s through immediate, efficient vaccination.
  • In most places, however, this is not close to happening. And as of last week, only one of the world’s 29 poorest countries had vaccinated anyone at all. A study in the journal BMJ estimated that vaccines will not be available to more than a fifth of the world’s population until 2022.
  • The coronavirus’s constantly evolving nature is a stark reminder that the entire world is in this crisis together.
  • Vaccine distribution is more than just an issue of justice or morality
  • Ensuring that every human is vaccinated is in everyone’s interest, as global distribution of vaccines is the most effective way to drive down the virus’s capacity to replicate and evolve.
  • The key will be bringing down the global rates of transmission as quickly as possible—not getting any single country to 100 percent vaccination while dozens of countries roil.
  • “It is truly confounding that wealthier nations think that hoarding vaccines is the way to protect their citizens from a global pandemic that doesn’t respect borders,”
  • As the virus currently surges across Africa, some 2.5 million health-care workers are unvaccinated. “Clearly, the failure to address vaccine allocation based on health and epidemiological needs, rather than national interest, is now promising to have a dire impact on the world’s ability to achieve rapid, global control of COVID,”
  • Certain countries will approach herd immunity by vaccinating almost every citizen. Other countries could see mass casualties and catastrophic waves of reinfection—potentially with variants that evolved in response to the immunity conferred by the very vaccines to which these populations do not have access. In the process, these hot spots themselves will facilitate rapid evolution, giving rise to even more variants that could make the vaccinated populations susceptible to disease once again
  • The countries that hoard the vaccine without a plan to help others do so at their own peril.
xaviermcelderry

New Coronavirus Variants: What Mutations Mean for the Pandemic - The Atlantic - 0 views

  • In the final, darkest days of the deadliest year in U.S. history, the world received ominous news of a mutation in the SARS-CoV-2 coronavirus. Scientists in the U.K. had identified a form of the virus that was spreading rapidly throughout the nation. Then, on January 4, Prime Minister Boris Johnson announced a lockdown that began almost immediately and will last until at least the middle of February.
  • he said in an address, noting that “our scientists have confirmed this new variant is between 50 and 70 percent more transmissible” than previous strains.
  • Each day, B.1.1.7 is being found in more people in more places, including all around the United States. Experts have raised dire warnings that a 70 percent more transmissible form of the virus would overwhelm already severely stretched medical systems. Daily deaths have already tripled in recent months, and the virus is killing more than 3,000 Americans every day. From a purely mathematical perspective, considering exponential growth, a significantly more transmissible strain could theoretically lead to tens of thousands of daily deaths, with hospital beds lining sidewalks and filling parking lots.
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  • Almost all of these accidental mutations are inconsequential: The virus still looks and functions just as its parent before it did. Over time, though, sets of mutations can layer on top of one another and accumulate, and the virus begins to function differently. Some of these differences confer an advantage of one sort or another—for example, increased transmissibility.
  • He has been at the forefront of identifying and tracking the variant, but says huge questions remain unanswered. “There’s still considerable uncertainty as to the long-term consequences” of B.1.1.7, Pybus told me. “We don’t even know whether this lineage truly originated in the U.K., with so many countries not doing this surveillance.”
Javier E

What the Future May Hold for the Coronavirus and Us - The New York Times - 0 views

  • the appearance of more transmissible variants is textbook viral evolution.
  • “If you change that shape, you can make it impossible for an antibody to do its job,”
  • There are likely to be some basic biological limits on just how infectious a particular virus can become, based on its intrinsic properties. Viruses that are well adapted to humans, such as measles and the seasonal influenza, are not constantly becoming more infectious,
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  • “Whether the Delta variant is already at that plateau, or whether there’s going to be further increases before it gets to that plateau, I can’t say. But I do think that plateau exists.”
  • Antibodies, which can prevent the virus from entering our cells, are engineered to latch onto specific molecules on the surface of the virus, snapping into place like puzzle pieces. But genetic mutations in the virus can change the shape of those binding sites.
  • “It’s hard to imagine that the virus is going to pop into a new species perfectly formed for that species,” said Andrew Read, an evolutionary microbiologist at Penn State University. “It’s bound to do some adaptation.”
  • But as more people acquire antibodies against the virus, mutations that allow the virus to slip past these antibodies will become even more advantageous.
  • The good news is that there are many different kinds of antibodies, and a variant with a few new mutations is unlikely to escape them all, experts said.
  • its sleeve to counteract the evolution of the virus,” Dr. Pepper said. “Knowing that there is this complex level of diversity in the immune system allows me to sleep better at night.”
  • “It’s a lot harder to evade T cell responses than antibody responses,”
  • And then there are B cells, which generate our army of antibodies. Even after we clear the infection, the body keeps churning out B cells for a while, deliberately introducing small genetic mutations. The result is an enormously diverse collection of B cells producing an array of antibodies, some of which might be a good match for the next variant that comes along.
  • Unlike transmissibility or immune evasion, virulence has no inherent evolutionary advantage.
  • Whether the virus will become more virulent — that is, whether it will cause more serious disease — is the hardest to predict,
  • Some scientists predict that the virus will ultimately be much like the flu, which can still cause serious illness and death, especially during seasonal surges.
  • “The virus has no interest in killing us,” Dr. Metcalf said. “Virulence only matters for the virus if it works for transmission.”
  • So far, studies suggest that our antibody, T cell and B cell responses are all working as expected when it comes to SARS-CoV-2. “This virus is mostly playing by immunological rules we understand,”
  • Then again, this virus spreads before people become severely ill. As long as that remains true, the virus could become more virulent without sacrificing transmissibility.
  • Moreover, the same thing that makes the virus more infectious — faster replication or tighter binding to our cells — could also make it more virulent.
  • Although many possible paths remain open to us, what is certain is that SARS-CoV-2 will not stop evolving — and that the arms race between the virus and us is just beginning.
  • We lost the first few rounds, by allowing the virus to spread unchecked, but we still have powerful weapons to bring to the fight. The most notable are highly effective vaccines, developed at record speed. “I think there is hope in the fact that the SARS-CoV-2 vaccines at this point are more effective than flu vaccines have probably ever been,”
  • “I have great faith that we can sort any detrimental evolutionary trajectories out by improving our current or next generation vaccines,”
  • be you have a re-infection, but it’s relatively mild, which also boosts your immunity,”
  • rising vaccination rates may already be suppressing new mutations.And the evolution rate could also slow down as the virus becomes better adapted to humans.
  • “There’s low-hanging fruit,” Dr. Lauring said. “So there are certain ways it can evolve and make big improvements, but after a while there aren’t areas to improve — it’s figured out all the easy ways to improve.”
  • Eventually, as viral evolution slows down and our immune systems catch up, we will reach an uneasy equilibrium with the virus, scientists predict. We will never extinguish it, but it will smolder rather than rage.
  • It is too early to say whether SARS-CoV-2 will change in virulence over the long-term. There could certainly be trade-offs between virulence and transmission; variants that make people too sick too quickly may not spread very far.
  • Others are more optimistic. “My guess is that one day this is going to be another cause of the common cold,”
  • There are four other coronaviruses that have become endemic in human populations. We are exposed to them early and often, and all four mostly cause run-of-the-mill colds.
  • much of the world remains unvaccinated, and this virus has already proved capable of surprising us. “We should be somewhat cautious and humble about trying to predict what it is capable of doing in the future,”
  • While we can’t guard against every eventuality, we can tip the odds in our favor by expanding viral surveillance, speeding up global vaccine distribution and tamping down transmission until more people can be vaccinated
  • The future, he said, “depends much, much more on what humans do than on what the virus does.”
Javier E

Lung Samples From 1918 Show a Pandemic Virus Mutating - The Atlantic - 0 views

  • Why was the second wave, in late 1918, so much deadlier than the first wave, in the spring? These rediscovered lung samples hint at the possibility that the virus itself changed to better infect humans.
  • This new study brings the number of complete 1918 flu genomes to a grand total of three, plus some partial genomes.
  • Several changes showed up in the flu’s genome-replication machinery, a potential evolutionary hot spot because better replication means a more successful virus. The team then copied just the replication machinery of the 17-year-old’s virus—not the entire virus—into cells and found it was only half as active as that of the flu virus found in Alaska.
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  • Bloom and others have identified specific mutations that make the nucleoprotein better at resisting the human immune system. The first-wave flu viruses did not have them, but the second-wave ones did, possibly because they had had the time to adapt to infecting humans.
  • This mutation-by-mutation analysis of the 1918 flu virus would have been impossible to imagine at the time of the pandemic. Doctors then hadn’t even figured out that influenza was caused by a virus. “There’s no way the individual who saved these samples in 1918 had any idea of what could be done to them,” Mehle said. “To my mind, this is a beautiful example of fundamental research.”
  • Without the pathologist who painstakingly preserved these samples and the museums that kept them for decades before science caught up, our understanding of the 1918 flu would be all the poorer.
  • When the 1918 pandemic swept through the world, it apparently completely replaced whatever flu existed before. Its modern-day descendants continue to infect us today as seasonal flu.
Javier E

Genetic sequencing: U.S. lags behind in key tool against coronavirus mutations - The Wa... - 0 views

  • The lack of widespread genetic sequencing means the window is closing to find and slow the spread of variants such as the one first spotted in Britain, which appears to be much more transmissible, and those initially detected in Brazil and South Africa. All have been discovered in small numbers in the United States.
  • Now is when genetic sequencing — a process that maps out the genetic code of the particular virus that infected someone so it can be compared with others — would do the most good, while such variants are less prevalent in the U.S. population and action can be taken against them.
  • “We are in a race against time because of these mutations. And in that race, we are falling behind,”
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  • The problem echoes the country’s catastrophic stumbles early in the pandemic, when a lack of testing allowed the virus to spread widely. Currently, only a tiny fraction of all positive coronavirus tests in the United States are forwarded for further sequencing.
  • t if scientists don’t know what strains are moving through the population, the mutations that matter may pop up undetected.
  • For months, scientists have been sounding alarms and trying to ramp up genetic sequencing of test samples, but the effort has been plagued by a lack of funding, political will and federal coordination
  • Centers for Disease Control and Prevention Director Rochelle Walensky said Friday that the government is increasing the level of sequencing nationwide.“We have scaled up surveillance dramatically just in the last 10 days, in fact. But our plans for scaling up surveillance are even more than what we’ve done so far,”
  • Ultimately, the country needs real-time data — similar to the dashboards now used to track daily cases, hospitalizations and deaths — to track variants and their prevalence across the country
  • “None of that exists right now. We’re incredibly behind compared to other countries,”
  • The U.S. effort is so underdeveloped that it’s impossible to say exactly how many virus cases are sequenced daily.
  • The CDC has warned that the variant found in the United Kingdom — which British scientists said could be up to 70 percent more transmissible — could become dominant in the United States by March.
  • It also recently contracted with four private companies — Quest, Labcorp, Illumina and Helix — to conduct more sequencing. By mid-February, those contracts should hit full capacity, analyzing 6,000 samples per week, CDC officials said.
  • Illumina estimates that the country needs to sequence 5 percent of its coronavirus cases to detect a new variant when the variant represents about 0.1 percent to 1.0 percent of the country’s case
  • However, the United States so far has only sequenced about 0.32 percent of its total cases
  • the country ranks 38th out of 130 countries reporting whole-genome sequencing data.
  • The United States has sequenced 84,177 samples out of 25.7 million cases as of Friday, according to a Washington Post analysis. By comparison, the United Kingdom, in ninth place, has sequenced 214,000 genomes — almost 6 percent — of the country’s 3.7 million cases.
  • Unlike the United States, the U.K. invested in genetic sequencing early on in the pandemic, launching its genomics consortium in March with a $27 million investment and a multimillion-dollar boost late last year.
  • Even before the emergence of mutations such as the variants first discovered in South Africa and the United Kingdom, U.S. experts had been warning for months about the need for a national standard for genetic surveillance.
  • In May, the CDC launched a surveillance program for the coronavirus called SPHERES (SARS-CoV-2 Sequencing for Public Health Emergency Response, Epidemiology, and Surveillance). But, in practice, the program relied on a haphazard patchwork of academic labs contributing genetic sequencing on a volunteer basis.
  • A July report by the National Academies of Science said that “poor funding, coordination, and capacity” had led to a “patchy, typically passive, and reactive” U.S. sequencing effort.
aidenborst

Tests Show Genetic Signature of Coronavirus That Likely Infected Trump - The New York T... - 0 views

  • President Trump’s illness from a coronavirus infection last month was the most significant health crisis for a sitting president in nearly 40 years. Yet little remains known about how the virus arrived at the White House and how it spread
  • The administration did not take basic steps to track the outbreak, limiting contact tracing, keeping cases a secret and cutting out the Centers for Disease Control and Prevention. The origin of the infections, a spokesman said, was “unknowable.”
  • The journalists, Michael D. Shear and Al Drago, both had significant, separate exposure to White House officials in late September, several days before they developed symptoms. They did not spend any time near each other in the weeks before their positive tests.
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  • The study reveals, for the first time, the genetic sequence of the virus that may have infected Mr. Trump and dozens of others, researchers said.
  • Viruses constantly mutate, picking up tiny, accidental alterations to their genetic material as they reproduce. Few mutations alter how a virus functions. But by comparing patterns of mutations across many genetic sequences, scientists can construct family trees of a virus, illuminating how it spreads.
  • The genomes believed by these researchers to be connected to the White House outbreak do not identify a recent geographic source, in part because they are unusual.
  • The results show that even weeks after it was identified, the White House outbreak would be better understood by sequencing samples of more people who were infected.
  • In a study released on Thursday, the C.D.C. cited genetic sequencing and intensive contact tracing that documented an super-spreading event at a high school retreat in Wisconsin.
  • But the Trump administration is not known to have conducted its own genetic analysis of people infected in the outbreak. The White House declined to respond to questions on genetic sequencing of Mr. Trump and the cluster of aides and officials who tested positive or became ill.
  • Scientists not involved in the research who reviewed the results agreed with the conclusion that the two samples sharing rare mutations strongly suggested they are part of the same outbreak.
  • “These genomes are probably going to be identical or nearly identical to the genome that infected the president,” said Michael Worobey, head of the department of ecology and evolutionary biology at the University of Arizona.
  • For months, the White House minimized the threat of the virus and eschewed basic safety precautions at official events, like wearing a mask or keeping people six feet apart.
  • At least 11 people who attended a Rose Garden celebration on Sept. 26 for Judge Barrett, which included an indoor event without masks, became infected with the coronavirus, including Mr. Trump.
  • The work is convincing, and it is the best way to piece together the progression of such an outbreak, said David Engelthaler, head of the infectious disease branch of the Translational Genomics Research Institute in Arizona, where he and colleagues have sequenced thousands of genomes to track the spread of the coronavirus, including devastating outbreaks at Native American reservations in the state.
Javier E

China's New COVID Crisis Could Spawn the Worst Variant Yet - 0 views

  • Then came Omicron. The new lineage, which first appeared in South Africa last fall, is by far the most transmissible. Some experts described the earlier form of Omicron, the BA.1 sublineage, as the most contagious respiratory virus they’d ever seen, owing in part to key mutations on the spike protein, the part of the virus that helps it grab onto and infect human cells.
  • The BA.2 sublineage that soon replaced BA.1 is even worse: potentially 80 percent more contagious than BA.1. There’s also a very rare “recombinant” form of Omicron called XE that combines the qualities of BA.1 and BA.2 and might be 10 percent more transmissible than even BA.2.
  • even if they are reasonably effective, the vaccines are unevenly distributed in China. The government’s attacks on foreign jabs has had the effect of encouraging anti-vax attitudes, especially among older Chinese who might be less media-savvy than their younger counterparts.
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  • The virus kept spreading. By early April officials were logging an average of around 15,000 new cases a day. A spike in deaths followed. In Hong Kong alone, nearly 9,000 people have died since mid-February. To be clear, that’s a fraction of the infections and deaths that countries with fewer restrictions tallied during the worst of their own COVID surges. What’s so worrying in China is the trend—and the potential for cases, and deaths, to keep going up and up.
  • “It could be that we are seeing the resurgences in China, including the emergence and spread of new sub-strains, primarily because the population there never achieved high levels of natural immunity,”
  • You can’t build up natural antibodies across a large population if no one is ever exposed to the virus. That’s the downside of total lockdowns
  • The antibodies in recovered COVID patients lend strong immunity that, combined with vaccinations across large groups of people, can help blunt the impact of a new lineage. Michael for one said he believes natural immunity is stronger and longer-lasting than immunity resulting from even the best messenger-RNA vaccines.
  • “They also used inactivated viruses in their Sinovac and Sinopharm vaccines, which I had expected to be more robust than mRNA vaccines in terms of producing a more diversified immune response that could counter new mutants, et cetera,” Michael said, “but apparently it would seem that this response has waned, making people susceptible again to new strains.”
  • BA.1 and BA.2 shrugged off China’s strict social distancing. Even the most fleeting contact between family members, neighbors and coworkers was enough to ignite a viral firestorm in China starting in January.
  • just half of the most vulnerable age group–over-80s–is fully vaccinated. That plus the lack of natural immunity has left millions of Chinese exposed to aggressive lineages that can punch right through lockdowns.
  • . “Any place can be a source of new variants, but those places with low levels of population immunity and unchecked spread of the virus are the most likely,”
  • Each individual infection, unchecked by antibodies, tends to produce two mutations every two weeks,
  • “What if we had 50 million people pull slot-machine levers simultaneously at the same time?” Moshiri asked. “We would expect at least one person would hit the jackpot pretty quickly. Now, replace the slot machine with ‘clinically-meaningful SARS-CoV-2 mutation,’ and that’s the situation we're in.”
  • All that is to say, the longer COVID rates remain high in the world’s most-populous country, the greater the chance that the next major lineage will be Chinese.
  • New lineages are inevitable from one country or another, of course. The trick is to slow the rate of mutation so that fresh vaccine formulations, therapies and public-health policies can at least keep pace with major changes in the virus.
  • billion people with uneven rates of vaccination by potentially low-quality jabs and very little natural immunity to back up the shots.
Javier E

Tracing Ancestry, Researchers Produce a Genetic Atlas of Human Mixing Events - NYTimes.com - 0 views

  • geneticists applying new statistical approaches have taken a first shot at both identifying and dating the major population mixture events of the last 4,000 years, with the goal of providing a new source of information for historians.
  • Some of the hundred or so major mixing events they describe have plausible historical explanations, while many others remain to be accounted for.
  • many populations of the southern Mediterranean and Middle East have segments of African origin in their genomes that were inserted at times between A.D. 650 and 1900, according to the geneticists’ calculations. This could reflect the activity of the Arab slave trade,
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  • The lowest amount of African admixture occurs in the Druse, a religious group of the Middle East that prohibited slavery and has been closed to converts since A.D. 1043.
  • Another mixing event is the injection of European-type DNA into the Kalash, a people of Pakistan, at some time between 990 and 210 B.C. This could reflect the invasion of India by Alexander the Great in 326 B.C. The Kalash claim to be descended from Alexander’s soldiers
  • Though all humans have the same set of genes, their genomes are studded with mutations, which are differences in the sequence of DNA units in the genome. These mutations occur in patterns because whole sets of mutations are passed down from parent to child and hence will be common in a particular population
  • The dating system is based on measuring the length of chromosome segments of a particular ancestry that occur in a population. When people of two different populations intermarry, their children’s genomes carry large chunks of DNA of one parent’s ancestry interspersed with large chunks from the other’s.
  • from the average size of the chunks in a person’s genome, the geneticists can calculate the number of generations since the mixing event.
  • One of the most widespread events his group has detected is the injection of Mongol ancestry into populations within the Mongol empire, such as the Hazara of Afghanistan and the Uighur Turks of Central Asia.
  • the European colonization of America is recorded in the genomes of the Maya and Pima Indians. And Cambodian genomes mark the fall of the Khmer empire in the form of ancestral DNA from the invading Tai people.
  • They find among Northern Italians an insertion of Middle Eastern DNA that occurred between 776 B.C. and A.D. 550, and may represent the Etruscans, a mysterious people said by the ancient Greek historian Herodotus to have emigrated from Lydia in Turkey.
  • his method cannot yet detect genetic mixing between very similar populations, as was the case with the English and their invaders from Scandinavia and Northern Germany.
  • “In some sense we don’t want to talk to historians,” Dr. Falush said. “There’s a great virtue in being objective: You put the data in and get the history out. We do think this is a way of reconstructing history by just using DNA.”
carolinehayter

Messenger RNA vaccines: Now proven against coronavirus, the technology can do so much m... - 0 views

  • This astonishing efficacy has held up in real-world studies in the US, Israel and elsewhere. The mRNA technology -- developed for its speed and flexibility as opposed to expectations it would provide strong protection against an infectious disease -- has pleased and astonished even those who already advocated for it.
  • it's a technology that researchers had been betting on for decades. Now those bets are paying off, and not just by turning back a pandemic that killed millions in just a year.
  • showing promise against old enemies such as HIV, and infections that threaten babies and young children, such as respiratory syncytial virus (RSV) and metapneumovirus. It's being tested as a treatment for cancers, including melanoma and brain tumors. It might offer a new way to treat autoimmune diseases. And it's also being checked out as a possible alternative to gene therapy for intractable conditions such as sickle cell disease.
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  • "If you want to make a new influenza vaccine using the traditional methods, you have to isolate the virus, learn how to grow it, learn how to inactivate it, and purify it. That takes months. With RNA, you only need the sequence,"
  • "When the Chinese released the sequence of the SARS-CoV-2 virus, we started the process of making RNA the next day. A couple weeks later, we were injecting animals with the vaccine."
  • Weissman's lab is now working on a universal coronavirus vaccine that would protect against Covid-19, SARS, MERS, coronavirus that cause the common cold -- and future strains.
  • "We started working on a pan-coronavirus vaccine last spring," Weissman said. "There have been three coronavirus epidemics in the past 20 years. There are going to be more."
  • The mRNA approach promises to send instructions for making the healthy version of a protein, and Weissman sees special promise in treating sickle cell disease, in particular.
  • Different tumor cell types have various, recognizable structures on the outside that the immune system can recognize. "You can imagine being able to inject someone with an mRNA that encodes an antibody that specifically targets that receptor," McLellan said.
  • "We identify mutations found on a patient's cancer cells," the company says on its website. Computer algorithms predict the 20 most common mutations. "We then create a vaccine that encodes for each of these mutations and load them onto a single mRNA molecule," Moderna says.
  • BioNtech has been working with academic researchers to use mRNA to treat mice genetically engineered to develop a disease similar to multiple sclerosis -- an autoimmune disease that starts when the immune system mistakenly attacks the myelin, a fatty covering of the nerve cells.In the mice, the treatment appeared to help stop the attack, while keeping the rest of the immune system intact.
  • The idea behind gene therapy is to replace a defective gene with one that works properly.
  • Another obvious use for mRNA technology is to fight cancer. The human body fights off cancer every day, and using mRNA could help it do so even better.
  • "It's gene therapy without the half a million dollar price tag," he added. "It should be just an IV injection and that's it."
  • "The idea there is if you are immune to tick saliva proteins, when the tick bites you, the body produces inflammation and the tick falls off," Weissman said.
Javier E

Listen: Coronavirus Mutations - The Atlantic - 0 views

  • this gets to a weird aspect of disease and transmissibility. If you get really sick, you actually don’t transmit the virus all that well because you’re really sick and you don’t interact with the same number of people, whereas a virus that causes less disease might actually be more transmissible in a sense, because, since you don’t feel as bad, you’re more likely to transmit it to other people.
  • So there’s a bit of a dichotomy in how viruses spread. This particular COVID-19 is kind of this Goldilocks of viruses. If it was a little bit more severe, it would be easier to control. If it was a little bit less severe, it wouldn’t be as disruptive.
  • These variants we’re seeing haven’t been pushed to evolve away from antibodies yet.
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  • Your antibodies may be not as effective, but they’re still going to be effective. If you have 10 times the amount of antibody that you need and you lose half of that, you’re still going to be well protected. And I think that’s where these variants are. Most people will be well protected from the worst aspects of disease.
  • There are four or five common-cold coronaviruses. Many of them have their roots in animals, whether they be bats or cows or other animal species, and then jumped into humans. None of those viruses cause severe disease. They’re all relatively transmissible, and you can get infected every two or three years with them.
  • There is some possibility [SARS-CoV-2] will go along that route. Once we’ve all gotten some level of baseline immunity—we’ve seen a virus like this or very similar to this—the next time you have it, it [may cause] a mild infection but, for the most part, you won’t end up in a hospital or on a respirator. That’s kind of the trajectory that you could expect, but again, we don’t know.
  • This event could have happened in 2002 with [SARS-CoV-1], but that virus was effectively stopped through quarantining and other procedures. We have an event now where most of the world will have seen this virus, either through a vaccine or through natural immunity, and so its trajectory in a few years is really hard to predict. I’m hopeful that it’s going to be more like a common-cold coronavirus. The best outcome would be that it’s like SARS 1 and it just disappears from the Earth.
anonymous

Covid: How worrying are the UK, South Africa, and Brazil coronavirus variants? - 0 views

  • Experts' concerns currently focus on a small number of new variants of coronavirus:A UK variant that has become dominant in much of Britain and has spread to more than 50 other countriesA South Africa variant that has also been found in at least 20 other countries, including the UKA variant from BrazilIt's not unexpected that new variants have developed - all viruses mutate as they make new copies of themselves to spread and thrive.
  • Most of these differences are inconsequential. A few can even be harmful to the virus's survival.
  • It's suspected that the UK, South Africa and Brazil variants could be much more contagious or easy to catch than earlier versions. All three have undergone changes to their spike protein - this is the part of the virus which attaches to human cells.
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  • Experts think the UK or "Kent" strain emerged in September and may be up to 70% more transmissible or infectious, although latest research by Public Health England puts it between 30% and 50%.
  • The South Africa variant emerged in October, and it has more potentially important changes in the spike protein than the UK variant. It has one of the same mutations as the UK one, plus two more that scientists think may interfere more with vaccine effectiveness. One of these may help the virus evade parts of the immune system called antibodies.The UK has imposed a ban on direct flights from South Africa and restrictions on flights to the country.
  • The Brazil variant emerged in July and has three key mutations in the spike protein that make it similar to the South Africa one.
  • The current vaccines were designed around earlier variants, but scientists are confident that they should still work against the new ones, although perhaps not quite as well.
  • Vaccines train the body to attack several parts of the virus, however, not just these sections of the spike protein. Variants could emerge in the future that are more different again.Even in the worst case scenario, the vaccines could be redesigned and tweaked to be a better match - in a matter or weeks or months, if necessary,
  • As with flu vaccines, where a new shot is given each year to account for any changes in circulating flu viruses, something similar could happen for coronavirus.
  • There is currently no evidence to suggest that any of them cause more serious illness.Measures such as washing your hands, keeping your distance from other people and wearing a face covering will still help prevent infections, and because the new variants spread more easily it is important to be extra vigilant.
  • Scientists around the world are on the look-out and any new variants will be closely studied and monitored. Researchers at the Kenya Medical Research Institute say they are analysing a new variant that is different to the UK and South Africa strains, for example. The UK's vaccine development minster Nadhim Zahawi says measures have already been put in place to produce another wave of vaccines if needed.
martinelligi

These coronavirus variants are keeping scientists awake at night - CNN - 0 views

  • One, first identified in southeast England, has now shown up in at least 50 countries and appears to be spreading more efficiently than older variations of the virus. Its appearance has frightened political leaders, who have closed borders and imposed travel restrictions in attempts to curb its spread.
  • So far, none has done what scientists most fear and mutated to the point that it causes more severe disease, or evades the protection provided by vaccination. While some of the new variants appear to have changes that look like they could affect immune response, it's only by a matter of degree.
  • At the top of the list for researchers in the US is the B.1.1.7 variant first seen in Britain. The US Centers for Disease Control and Prevention warned last week it could worsen the spread of the pandemic.
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  • "Contacts of people with B.1.1.7 would get sicker at higher rates."
  • Plus there's evidence people infected with the B.1.1.7 variant have what's known as a higher viral load -- they have more virus reproducing in their bodies. That makes sense if the variant infects cells more easily, because viruses hijack the cells they infect, turning them into virus factories. More infected cells equal more virus.
  • Biologist Michael Worobey of the University of Arizona said he's found evidence B.1.1.7 was imported at least five separate times to the US, and likely many more. "It is striking that this lineage may already have been established in the US for some 5-6 weeks before B.1.1.7 was first identified as a variant of concern in the UK in mid-December,"
  • That should reassure people, Nussenzweig said. The human immune system adapts very well to viral mutations, he said, and produces hundreds of different antibodies that can attack coronavirus.
  • Finally, there's a new variant seen in California. "We don't know yet what the significance of that one is," said Armstrong. It also has a mutation in the receptor binding domain of the spike protein. The new California variant is called L425R and while it's being found commonly, it's not yet clear if it's more transmissible.
mimiterranova

Contagious Coronavirus Variant Has Spread To Dozens Of Countries : Coronavirus Updates ... - 0 views

  • The U.S. has hit another devastating milestone: COVID-19 has killed more than 350,000 people in the country, according to a Johns Hopkins University tracker.
  • The variant is now in dozens of countries, including the United States, where it has infected people in Colorado, California and Florida.
  • Researchers say the new variant — dubbed B.1.1.7 — probably originated in the South East region of England in Septembe
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  • bly originated in the South East region of England in Septembe
  • The World Health Organization says the new variant is responsible for more than half of new infections in the U.K.
  • And the new version of the virus is already mutating — 17 mutations have been spotted
  • "In the vast majority of cases, these mistakes are harmless or they even weaken the virus," Doucleff said. "But in rare instances, mutations can help the virus — they can give it this little boost, or advantage, over the other versions."
  • The good news is that the new variant doesn't appear to be more deadly. But it is much more contagious — researchers are still trying to determine exactly how much more, but many have estimated it could be 50% more transmissible than the original strain
anonymous

The U.K. Variant Seems More Contagious. What Precautions Should I Take? : Goats and So... - 0 views

  • While COVID-19 has mutated in thousands of mostly harmless ways, the world is increasingly focused on one variant detected in England, dubbed B.1.1.7, and one found in South Africa, called 501.V2, because they seem to spread more easily than older strains.
  • A dramatic rise in B.1.1.7 cases, especially in southeast London, made experts wonder if the new strain could be more infectious. While researchers are still trying to tease apart whether that's the case, or whether the rise could be attributed to a sociological change such as people mixing for the holidays, there are some biological reasons that make this strain easier to spread,
  • A top hypothesis that this strain is more infectious comes from a study looking at how much virus a person generates in the nose.
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  • so that when they cough, sneeze, talk or scream, they likely expel more virus into the air. More virus in the air likely means you infect more people around you.
  • Less is known about the South African strain, but at least one of its mutations appears to alter the spike protein. So stricter steps, such as lockdowns and border controls, may be necessary to curtail spread, say experts who live in current hot spots.
  • In lieu of government action, it may be best to avoid other people as much as possible
  • "One of the big problems is people thinking as individuals and not as a global population,
  • The actions of one person have the potential for enormous impact on people they've never met.
  • Yes and no, experts say. If you've been following the oft-repeated safety protocols to the letter, you might not have much adjusting to do.
  • Despite pandemic fatigue, this is not the time for slacking, the prevention specialists say.
  • When it's your turn, get your vaccine as soon as you can.
  • "It's important to really follow through and be as much of a stickler as you can for the recommendations,"
  • There is an upside. If we are actually able to adhere to strict protocols, we'd be rewarded with more than personal protection, Squires says. A virus mutates when its RNA is incorrectly copied in a host.
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