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one of the leading modelers, Gabriela Gomes, suggested the entire area of research was being effectively blackballed out of fear it might encourage a relaxation of pandemic vigilance. “This is the very sad reason for the absence of more optimistic projections on the development of this pandemic in the scientific literature,” she wrote on Twitter. “Our analysis suggests that herd-immunity thresholds are being achieved despite strict social-distancing measures.”

Gomes suggested, herd immunity could happen with as little as one quarter of the population of a community exposed — or perhaps just 20 percent. “We just keep running the models, and it keeps coming back at less than 20 percent,” she told Hamblin. “It’s very striking.” Such findings, if they held up, would be very instructive, as Hamblin writes: “It would mean, for instance, that at 25 percent antibody prevalence, New York City could continue its careful reopening without fear of another major surge in cases.”

But for those hoping that 25 percent represents a true ceiling for pandemic spread in a given community, well, it almost certainly does not, considering that recent serological surveys have shown that perhaps 93 percent of the population of Iquitos, Peru, has contracted the disease; as have more than half of those living in Indian slums; and as many as 68 percent in particular neighborhoods of New York City

overshoot of that scale would seem unlikely if the “true” threshold were as low as 20 or 25 percent.

But, of course, that threshold may not be the same in all places, across all populations, and is surely affected, to some degree, by the social behavior taken to protect against the spread of the disease.

we probably err when we conceive of group immunity in simplistically binary terms. While herd immunity is a technical term referring to a particular threshold at which point the disease can no longer spread, some amount of community protection against that spread begins almost as soon as the first people are exposed, with each case reducing the number of unexposed and vulnerable potential cases in the community by one

you would not expect a disease to spread in a purely exponential way until the point of herd immunity, at which time the spread would suddenly stop. Instead, you would expect that growth to slow as more people in the community were exposed to the disease, with most of them emerging relatively quickly with some immune response. Add to that the effects of even modest, commonplace protections — intuitive social distancing, some amount of mask-wearing — and you could expect to get an infection curve that tapers off well shy of 60 percent exposure.

Looking at the data, we see that transmissions in many severely impacted states began to slow down in July, despite limited interventions. This is especially notable in states like Arizona, Florida, and Texas. While we believe that changes in human behavior and changes in policy (such as mask mandates and closing of bars/nightclubs) certainly contributed to the decrease in transmission, it seems unlikely that these were the primary drivers behind the decrease. We believe that many regions obtained a certain degree of temporary herd immunity after reaching 10-35 percent prevalence under the current conditions. We call this 10-35 percent threshold the effective herd immunity threshold.

Indeed, that is more or less what was recently found by Youyang Gu, to date the best modeler of pandemic spread in the U.S

he cautioned again that he did not mean to imply that the natural herd-immunity level was as low as 10 percent, or even 35 percent. Instead, he suggested it was a plateau determined in part by better collective understanding of the disease and what precautions to take

Gu estimates national prevalence as just below 20 percent (i.e., right in the middle of his range of effective herd immunity), it still counts, I think, as encouraging — even if people in hard-hit communities won’t truly breathe a sigh of relief until vaccines arrive.

If you can get real protection starting at 35 percent, it means that even a mediocre vaccine, administered much more haphazardly to a population with some meaningful share of vaccination skeptics, could still achieve community protection pretty quickly. And that is really significant — making both the total lack of national coordination on rollout and the likely “vaccine wars” much less consequential.

At least 20 percent of the public, and perhaps 50 percent, had some preexisting, cross-protective T-cell response to SARS-CoV-2, according to one much-discussed recent paper. An earlier paper had put the figure at between 40 and 60 percent. And a third had found an even higher prevalence: 81 percent.

The T-cell story is similarly encouraging in its big-picture implications without being necessarily paradigm-changing

These numbers suggest their own heterogeneity — that different populations, with different demographics, would likely exhibit different levels of cross-reactive T-cell immune response

The most optimistic interpretation of the data was given to me by Francois Balloux, a somewhat contrarian disease geneticist and the director of the University College of London’s Genetics Institute

According to him, a cross-reactive T-cell response wouldn’t prevent infection, but would probably mean a faster immune response, a shorter period of infection, and a “massively” reduced risk of severe illness — meaning, he guessed, that somewhere between a third and three-quarters of the population carried into the epidemic significant protection against its scariest outcomes

the distribution of this T-cell response could explain at least some, and perhaps quite a lot, of COVID-19’s age skew when it comes to disease severity and mortality, since the young are the most exposed to other coronaviruses, and the protection tapers as you get older and spend less time in environments, like schools, where these viruses spread so promiscuously.

Balloux told me he believed it was also possible that the heterogeneous distribution of T-cell protection also explains some amount of the apparent decline in disease severity over time within countries on different pandemic timelines — a phenomenon that is more conventionally attributed to infection spreading more among the young, better treatment, and more effective protection of the most vulnerable (especially the old).

Going back to Youyang Gu’s analysis, what he calls the “implied infection fatality rate” — essentially an estimated ratio based on his modeling of untested cases — has fallen for the country as a whole from about one percent in March to about 0.8 percent in mid-April, 0.6 percent in May, and down to about 0.25 percent today.

even as we have seemed to reach a second peak of coronavirus deaths, the rate of death from COVID-19 infection has continued to decline — total deaths have gone up, but much less than the number of cases

In other words, at the population level, the lethality of the disease in America has fallen by about three-quarters since its peak. This is, despite everything that is genuinely horrible about the pandemic and the American response to it, rather fantastic.

there may be some possible “mortality displacement,” whereby the most severe cases show up first, in the most susceptible people, leaving behind a relatively protected population whose experience overall would be more mild, and that T-cell response may play a significant role in determining that susceptibility.

That, again, is Balloux’s interpretation — the most expansive assessment of the T-cell data offered to me

The most conservative assessment came from Sarah Fortune, the chair of Harvard’s Department of Immunology

Fortune cautioned not to assume that cross-protection was playing a significant role in determining severity of illness in a given patient. Those with such a T-cell response, she told me, would likely see a faster onset of robust response, yes, but that may or may not yield a shorter period of infection and viral shedding

Most of the scientists, doctors, epidemiologists, and immunologists I spoke to fell between those two poles, suggesting the T-cell cross-immunity findings were significant without necessarily being determinative — that they may help explain some of the shape of pandemic spread through particular populations, but only some of the dynamics of that spread.

he told me he believed, in the absence of that data, that T-cell cross-immunity from exposure to previous coronaviruses “might explain different disease severity in different people,” and “could certainly be part of the explanation for the age skew, especially for why the very young fare so well.”

the headline finding was quite clear and explicitly stated: that preexisting T-cell response came primarily via the variety of T-cells called CD4 T-cells, and that this dynamic was consistent with the hypothesis that the mechanism was inherited from previous exposure to a few different “common cold” coronaviruses

“This potential preexisting cross-reactive T-cell immunity to SARS-CoV-2 has broad implications,” the authors wrote, “as it could explain aspects of differential COVID-19 clinical outcomes, influence epidemiological models of herd immunity, or affect the performance of COVID-19 candidate vaccines.”

“This is at present highly speculative,” they cautioned.

“Usually by four to six weeks, there’s not much left,” said Deepta Bhattacharya, an immunologist at the University of Arizona. But germinal centers stimulated by the mRNA vaccines are “still going, months into it, and not a lot of decline in most people.”

The broader the range and the longer these cells have to practice, the more likely they are to be able to thwart variants of the virus that may emerge.

“Everyone always focuses on the virus evolving — this is showing that the B cells are doing the same thing,” said Marion Pepper, an immunologist at the University of Washington in Seattle. “And it’s going to be protective against ongoing evolution of the virus, which is really encouraging.”

Dr. Ellebedy’s team found that 15 weeks after the first dose of vaccine, the germinal center was still highly active in all 14 of the participants, and that the number of memory cells that recognized the coronavirus had not declined.

“The fact that the reactions continued for almost four months after vaccination — that’s a very, very good sign,” Dr. Ellebedy said. Germinal centers typically peak one to two weeks after immunization, and then wane.

After an infection or a vaccination, a specialized structure called the germinal center forms in lymph nodes. This structure is an elite school of sorts for B cells — a boot camp where they become increasingly sophisticated and learn to recognize a diverse set of viral genetic sequences.

The results suggest that a vast majority of vaccinated people will be protected over the long term — at least, against the existing coronavirus variants

But older adults, people with weak immune systems and those who take drugs that suppress immunity may need boosters; people who survived Covid-19 and were later immunized may never need them at all.

In the absence of variants that sidestep immunity, in theory immunity could last a lifetime, experts said. But the virus is clearly evolving.

“Anything that would actually require a booster would be variant-based, not based on waning of immunity,” Dr. Bhattacharya said. “I just don’t see that happening.”

The good news: A booster vaccine will probably have the same effect as prior infection in immunized people, Dr. Ellebedy said. “If you give them another chance to engage, they will have a massive response,” he said, referring to memory B cells.

Dr. Ellebedy said the results also suggested that these signs of persistent immune reaction might be caused by mRNA vaccines alone, as opposed to those made by more traditional means, like Johnson & Johnson’s

But that is an unfair comparison, because the Johnson & Johnson vaccine is given as a single dose, Dr. Iwasaki said: “If the J & J had a booster, maybe it will induce this same kind of response.”

She and others emphasized the apparent lack of severe health repercussions from reinfection — and the lack of evidence that reinfection is common.

Nearly 4 percent of people who had a previous infection were reinfected, an almost identical rate to those with no history of infection.

“Basically, it’s saying vaccination actually needs to be better than natural immunity. But vaccination is better than natural immunity.”

The study backs up recent laboratory data from South African researchers analyzing blood plasma from recovered patients. Nearly half of the plasma samples had no detectable ability to block the variant from infecting cells in a laboratory dish

The good news is that vaccine trials from Johnson & Johnson and Novavax show that vaccines can work — even against the B.1.351 variant, and particularly in preventing severe illness.

Novavax did not provide a breakdown of mild, moderate and severe cases, but severe cases of covid-19 were rare in the trial, suggesting that reinfection is unlikely to send people to the hospital.

“It is not surprising to see reinfection in individuals who are convalescent. And it would not be surprising to see infection in people who are vaccinated, especially a few months out from vaccine,”

“The key is not whether people get reinfected, it’s whether they get sick enough to be hospitalized.

“If the data holds true, it means we will need to walk the public back on the idea of how close we are to the finish line for ending this pandemic.”

Projections created by data scientist Youyang Gu — whose pandemic models have been cited by the Centers for Disease Control and Prevention — suggest that about 65 percent of America’s population will reach immunity by June 1. But built into that 65 percent is roughly 20 percent having immunity from past infections only.

In a separate study, scientists at Rockefeller University in New York took blood plasma from people who had been vaccinated and found that vaccine-generated antibodies were largely able to block mutations found on the B.1.351 variant.

I think the fact that we … now have data from two vaccines indicating that we can prevent serious disease, even against the new variant, is hopeful,”

A future concern needing close monitoring is whether the reformulation of vaccines to keep up with the evolving virus could drive the virus to continue evolving.

There is also a concern that subpar immunity could allow new resistant variants to emerge. That possibility, Nussenzweig said, is one reason that people should get both doses of a vaccine, on time.

That requires a high bar and makes it difficult to win unless the situation is similar to a prior case with nearly identical facts. In some cases with unique fact patterns, of which there are many, officers have been granted immunity even if they have been found to have acted in violation of the Constitution.

"Everyone has the potential for adverse encounters with state actors, whether it's members of law enforcement, public school officials, city council members, or other municipal employees," said Jay Schweikert, a policy analyst at the Cato Institute. "So long as the Supreme Court continues to permit this unlawful shield for government agents, no citizen will have any assurance that their rights will be respected."

"Until we shift the focus of our inquiry to whether immunity existed at common law, we will continue to substitute our own policy preferences for the mandates of Congress," the conservative Thomas wrote in a concurring opinion. "In an appropriate case, we should reconsider our qualified immunity jurisprudence."

In its 1982 decision, the court found that the aides were entitled to qualified immunity. "Government officials performing discretionary functions, generally are shielded from liability for civil damages insofar as their conduct does not violate clearly established statutory or constitutional rights of which a reasonable person would have known," the court ruled.

"The principle that government officials should be accountable for their violations of the Constitution is not a partisan issue. It's an American one," Boston University law professor Jack Beermann said in an interview with CNN. "Conservatives are just as concerned with abuse of government power as liberals are. And you combine that with what seems to be a rash of police misconduct in recent years and you can get a pretty strong coalition."

"There's an incredible urgency as communities across the country seek accountability for police violence against individuals of color in particularly, to open up the courts, claim a constitutional violation and make sure officers aren't provided a get-out-of-court-free card when they violate people's rights,"

"We are in the midst of a crisis of accountability in law enforcement,

As George Floyd's death tragically illustrates, for many people in this country, our culture of near-zero accountability for law enforcement is not an abstract public-policy concern, but a matter of life and death.

"At its heart, qualified immunity protects police officers' split second decisions ... courts must afford them a measure of deference in their on-the-scene assessments about the application of force to subdue a fleeing or resisting suspect,"

"Abandoning qualified immunity ... would leave hundreds of thousands of law enforcement officers exposed to potential liability, likely second guessing themselves in situations where a hesitation to act could mean the difference between life and death," the lawyers said in court papers.

Our case presents some of the problems with qualified immunity very starkly," said Michelman, lead counsel representing Baxter in the case. "Everyone should know, and everyone does know, that putting your hands up is a universal symbol of surrender and it is completely out of bounds to attack somebody who has surrendered."

"These cases very frequently arrive from police use of force in particular circumstances," Hughes said. "When an individual or his or her estate alleges that a police officer used excessive force the officer will invariably raise a qualified immunity defense."

“This virus has a surface protein that is primed to lock on that receptor and slip its RNA into the cell,”

Once inside, that RNA inserts itself into the cell’s own replication machinery and makes multiple copies of the virus. These burst out of the cell, and the infection spreads. Antibodies generated by the body’s immune system eventually target the virus and in most cases halt its progress.

“A Covid-19 infection is generally mild, and that really is the secret of the virus’s success,” adds Ball. “Many people don’t even notice they have got an infection and so go around their work, homes and supermarkets infecting others.”

the virus can cause severe problems. This happens when it moves down the respiratory tract and infects the lungs, which are even richer in cells with Ace-2 receptors. Many of these cells are destroyed, and lungs become congested with bits of broken cell. In these cases, patients will require treatment in intensive care.

Even worse, in some cases, a person’s immune system goes into overdrive, attracting cells to the lungs in order to attack the virus, resulting in inflammation

This process can run out of control, more immune cells pour in, and the inflammation gets worse. This is known as a cytokine storm.

Just why cytokine storms occur in some patients but not in the vast majority is unclear

Doctors examining patients recovering from a Covid-19 infection are finding fairly high levels of neutralising antibodies in their blood. These antibodies are made by the immune system, and they coat an invading virus at specific points, blocking its ability to break into cells.

Instead, most virologists believe that immunity against Covid-19 will last only a year or two. “That is in line with other coronaviruses that infect humans,

“It is clear that immune responses are being mounted against Covid-19 in infected people,” says virologist Mike Skinner of Imperial College London. “And the antibodies created by that response will provide protection against future infections – but we should note that it is unlikely this protection will be for life.”

“That means that even if most people do eventually become exposed to the virus, it is still likely to become endemic – which means we would see seasonal peaks of infection of this disease. We will have reached a steady state with regard to Covid-19.”

Skinner is doubtful. “We have got to consider this pandemic from the virus’s position,” he says. “It is spreading round the world very nicely. It is doing OK. Change brings it no benefit.”

In the end, it will be the development and roll-out of an effective vaccine that will free us from the threat of Covid-19,

the journal Nature reported that 78 vaccine projects had been launched round the globe – with a further 37 in development.

vaccines require large-scale safety and efficacy studies. Thousands of people would receive either the vaccine itself or a placebo to determine if the former were effective at preventing infection from the virus which they would have encountered naturally. That, inevitably, is a lengthy process.

some scientists have proposed a way to speed up the process – by deliberately exposing volunteers to the virus to determine a vaccine’s efficacy.

Volunteers would have to be young and healthy, he stresses: “Their health would also be closely monitored, and they would have access to intensive care and any available medicines.”

The result could be a vaccine that would save millions of lives by being ready for use in a much shorter time than one that went through standard phase three trials.

phase-three trials are still some way off, so we have time to consider the idea carefully.”

Way added that there might be other reasons why newborns should carry immunosuppressive cells

Baby formulas contain small amounts of arginine. Sidney Morris, a biochemist from the University of Pittsburgh, said that it may be important to avoid fortifying them with extra arginine, lest it swamps the arginase activity of CD71+ cells, releases the immune system, and causes problems for the developing infants’ guts.

“Whether the precise mechanism of immunosuppression is the same or different in each of these circumstances remains to be determined,” he said.

The new study provides “unassailable” evidence that the central nervous system can control the peripheral immune system, Tracey says. “It’s an incredibly important contribution to the fields of neuroscience and immunology.”

Just as researchers have traced sensory and motor processing to specific brain regions, Tracey suspects that a similar neurological “map” of immunologic information also exists. This new study, he says, is the first direct evidence of that map. “It’s going to be really exciting to see what comes next,” he adds.

. “Any successful virus has to get beyond that first defense system. The more successful it is at doing that, the better off the virus is.”

A lot of researchers focused their attention on the nine mutations that alter the so-called spike protein that covers the coronavirus and allows it to invade cells

They found that lung cells with Alpha made drastically less interferon, a protein that switches on a host of immune defenses.

It’s making itself more invisible,”

They found that Alpha-infected cells make a lot of extra copies — some 80 times more than other versions of the virus — of a gene called Orf9b.

dampening the production of interferon and a full immune response. The virus, protected from attack, has better odds of making copies of itself.

people infected with Alpha have a more robust reaction than they would with other variants, coughing and shedding virus-laden mucus from not only their mouths, but also their noses — making Alpha even better at spreading.

. They may have independently evolved their own tricks for manipulating our immune system.

But studies on people who recover naturally from Covid-19 have shown that their immune systems learn to recognize other viral proteins, including Orf9b.

“It’s quite a tricky enterprise, but becoming more possible as we learn more,”

The idea is textbook economics. People respond to incentives.

incentives can be used not just for the sake of individuals, but for the benefit of society as a whole.

it would be a drop in the bucket compared to the economic harm if the pandemic persists.

His plan would cost the country between $250 billion and $300 billion.

"Payments may indeed encourage some people to get the vaccine," says Cynthia Cryder, an associate professor of marketing at Washington University's Olin Business School. "But it may also deter people from getting the vaccine. Because payments signal that the vaccine is risky."

Another method of getting to herd immunity may exist, though it has not been discussed widely. Mandates — requiring people to get vaccinated either by orders of state governments or employers.

To economist Robert Litan, if we ultimately must choose between the carrot of cash payouts and the stick of mandated vaccines, the answer is clear: the carrot.

"I think the level of anger in the country will go up extraordinarily high if we had mandates," he says.

But one piece of advice almost no one is giving? Be lucky. Pediatrician Neil Stone says that there’s no “secret” for staying Covid-19 free because there’s just too much luck involved.

As for me, I have some data that can, to an extent, quantify and explain my own good luck in avoiding Covid so far. I’m participating in a study on immunity which allowed me to learn that my blood still carries loads of antibodies induced by my vaccine and December booster shot, and no signs of any prior infection. Not everyone’s antibodies wane at the same rate, and in some people, the antibodies don’t wane much at all. (At some point it should become routine to collect this information to help people decide whether to get additional booster shots.)

My high level of vaccine antibodies probably explains my success more than my behavior. I make some effort to avoid Covid, but have been far from perfect. And I’ve been potentially exposed at least twice: Once last December, when someone at a small holiday gathering I’d attended developed symptoms the next day, and more recently, when I shared a large indoor space with two people who later tested positive. But according to my lab work, I’ve never had even a silent infection.

It’s possible I was protected by my high antibodies, or that some quirk of air flow meant I never breathed in enough virus to get sick. Or perhaps I benefited from a different form of luck. There’s another facet to immunity called the innate immune system, which acts as a first line of defense and sometimes knocks out a virus or other pathogen before it replicates enough to elicit the production of antibodies. Good innate immunity might help explain something many of us have experienced — not getting a cold or flu even when sleeping in the same bed with the sick person through the whole illness.

Stress, diet, general health and even sunlight might all affect innate immunity. So could other factors. There’s so much we still don’t know about the immune system. And that’s one reason we talk about “luck.”

understanding how the luck works could help other people avoid Covid, whether for the first time or for the second or third time. Taking a closer look at what passed for luck helped researchers like Gary Taubes discover that public health had obesity all wrong, and the standard high carb/low fat diets were causing people to gain weight.

cross-reactive antibodies bind relatively weakly to their targets and, under normal circumstances, would probably get outcompeted by antibodies with a narrower focus but higher affinity. “For whatever reason, antibodies to the conserved regions are very rare,”

possible to skew the response towards more broadly cross-reactive antibodies, in mice, in a particular situation,”

not advocating that we use rapamycin [in humans],” said McGargill. However, her group’s discovery could point to other ways of achieving the same effect, perhaps by manipulating the immune system into producing more cross-reactive antibodies. “Maybe instead of trying to enhance the immune response, we need to dampen it a little bit, and allow it to be more diverse,

because the mutation is specific to the tumor — and can serve as a sort of beacon to properly designed immune cells — it might actually be this cancer's Achilles' heel.

treatment involves taking patients' T cells, then inserting a new gene that allows the cells to recognize the mutant protein.

the cells can be reinfused and begin their task of zeroing in on and eliminating cells with the mutation.

"It's taking an antibody, which is typically a kind of molecule that's circulating around in the blood," said Maus. "And it's fusing it to proteins that will cross the membrane and that then will signal to T cells to replicate and kill."

He is doing so, he said, partly based on new science, and partly on his gut feeling that the country is finally ready to hear what he really thinks.

Now that some polls are showing that many more Americans are ready, even eager, for vaccines, he said he felt he could deliver the tough message that the return to normal might take longer than anticipated.

We really don’t know what the real number is. I think the real range is somewhere between 70 to 90 percent.

not sure there will be enough voluntary acceptance of vaccines to reach that goal.

They also came with a warning: All answers are merely “guesstimates.”

Humans move around, so studying disease spread among them is far harder.

It took about two months to be certain that there were many asymptomatic people who had also spread the virus.

The more transmissible a pathogen, the more people must become immune in order to stop it.

Dr. Dean noted that to stop transmission in a crowded city like New York, more people would have to achieve immunity than would be necessary in a less crowded place like Montana.

If we can vaccinate almost all the people who are most at risk of severe outcomes, then this would become a milder disease.”

The agency cites the results of a study in Germany and clinical trials in the U.K. and Spain as supporting the safety of vaccine interchangeability.

As of late May, 50.6% of Canada's population had received at least one vaccination shot — but only 4.6% of the population was fully vaccinated.

"Different vaccine products have been used to complete a vaccine series for influenza, hepatitis A, and others to complete a vaccine series for influenza, hepatitis A, and others."

"Basically, all vaccines work by showing people's immune systems something that looks like an invading virus but really isn't. If the real virus ever comes along, their immune systems will recognize it and be prepared to fight it off.

"Using two different vaccines is a bit like giving the immune system two pictures of the virus, maybe one face-on and one in profile."

"Individuals who have received one dose of the Pfizer-BioNTech or Moderna COVID-19 vaccine should receive a second dose of the same vaccine to complete the vaccination series," the spokesperson added.

The human gut microbiome is diverse and dominated by trillions of bacteria with as many as one-thousand different bacterial species. These microbes thrive in the harsh conditions of the gut and are heavily involved in maintaining healthy nutrition, normal metabolism, and proper immune function. They aid in the digestion of non-digestible carbohydrates, the metabolism of bile acid and drugs, and in the synthesis of amino acids and many vitamins. A number of gut microbes also produce antimicrobial substances that protect against pathogenic bacteria.

Microbiota of the oral cavity number in the millions and include archaea, bacteria, fungi, protists, and viruses. These organisms exist together and most in a mutualistic relationship with the host, where both the microbes and the host benefit from the relationship. While the majority of oral microbes are beneficial, preventing harmful microbes from colonizing the mouth, some have been known to become pathogenic in response to environmental changes. Bacteria are the most numerous of the oral microbes and include Streptococcus, Actinomyces, Lactobacterium, Staphylococcus, and Propionibacterium.

How did immune cells get in, and how did they leave? No one knew.

The new study stands to resolve this and lead to new understanding of and treatments for vexing diseases.

For now, the researchers are hard at work on two major follow-up questions to try to figure out how the research might be relevant and useful. First, does this system definitely exist in humans? And second, what is the potential role of these vessels in Alzheimer's, MS, and meningitis?

The idea that an entire part of the lymphatic system was hiding in plain sight should ensure that these potentially crucial areas are ignored no longer. With any luck, this might help us solve more mysteries behind the brain — and fight some of its greatest foes.

The country will also need to open more vaccination sites, some of which should be open 24/7 to ensure people who get off work at odd hours have easy access to the vaccine.“This is a wartime sort of response,” Fagbuyi said. “You’re going to pull all the stops and not leave any stone unturned.”

“Enjoy the opportunity, but also be cautious and look at what’s going on around you,” Fagbuyi said.

“We’re going to be trying to convince people to come get vaccinated,” Adalja said.

Adalja predicts that by the Fourth of July, vulnerable people will be vaccinated in all states and there will no longer be concerns about reaching hospital capacity.

So, when will we get to a point where it won’t be so complicated for the general public to score a vaccine appointment? Fagbuyi predicts sometime in June.

We often hear doctors say we want 70% of the population to be immune to COVID-19, whether through vaccination, natural infection or preexisting immunity, to achieve herd immunity. Each dose pricked in someone’s arm makes it harder for the virus to spread.

“What I think is more important than herd immunity is making sure vulnerable populations are vaccinated so that COVID loses the ability to cause severe illness, hospitalization and death,” Adalja said.

“We have not seen any variants evade the vaccination completely,” Javaid said.

Right now we use antibody testing as a marker of an immune response. But we need more time to pass to study the population’s response to the vaccines before being able to sufficiently assess the duration of immunity.

The trial’s first participants, a pair of 9-year-old twin girls, were immunized at Duke University in North Carolina on Wednesday.

Immunizing children will help schools to reopen as well as help to end the pandemic, said Dr. Emily Erbelding, an infectious diseases physician at the National Institutes of Health who oversees testing of Covid-19 vaccines in special populations.

An estimated 80 percent of the population may need to be vaccinated for the United States to reach herd immunity, the threshold at which the coronavirus runs out of people to infect.

“we were encouraged by the data from the 12 to 15 group,

Scientists will test three doses of the Pfizer vaccine — 10, 20 and 30 micrograms — in 144 children. Each dose will be assessed first in children 5 through 11 years of age, then in children ages 2 through 4 years, and finally in the youngest group, six months to 2 years.

After determining the most effective dose, the company will test the vaccine in 4,500 children

“It sounds like a good plan, and it’s exciting that another Covid-19 vaccine is moving forward with trials in children,”

Children represent 13 percent of all reported cases in the United States.

More than 3.3 million children have tested positive for the virus, at least 13,000 have been hospitalized and at least 260 have died

“We don’t know what the long-term effects of Covid infection are going to be,” Dr. Maldonado said.

Other vaccines have helped to control many horrific childhood diseases that can cause long-term complications, she added: “For some of us who’ve seen that, we don’t want to go back to those days.”

“So there’s a higher degree of confidence now in giving this vaccine to kids.”

“The more transparent you can be, the better.”

I heard from young anthropologists, speaking the language of postmodernism, who consider science to be just another tool with which Western colonialism further extends its “cultural hegemony” by marginalizing the dispossessed and privileging its own worldview.

Science, through this lens, doesn’t discover knowledge, it “manufactures” it, along with other marketable goods.

The widening gyre of beliefs is accelerated by the otherwise liberating Internet. At the same time it expands the reach of every mind, it channels debate into clashing memes, often no longer than 140 characters, that force people to extremes and trap them in self-reinforcing bubbles of thought.