If Joe Biden beats Donald Trump this November and ends up in the Oval Office in January, he’ll quickly face one of the gravest challenges any president has seen in the modern era: Hundreds of thousands of Americans will be dead from Covid-19. Public trust in scientific and government institutions will be depleted. If the fall and winter goes as badly as some experts fear, coronavirus outbreaks may be at a new peak. And if a vaccine gets approved, it will still need to be distributed to hundreds of millions of Americans quickly and equitably.

Biden’s immediate job would be fixing the mess left behind by his predecessor — one that’s left America with one of the worst coronavirus outbreaks in the world and, as of September, more daily Covid-19 deaths than all but two developed countries.

Experts say these problems are fixable, but fixing them will largely come down to political will. The policy solutions are things that we’ve all heard about throughout the pandemic: aggressive testing and tracing to contain new outbreaks. Mask-wearing to slow the spread of the coronavirus. Economic support for those affected by the epidemic, at once providing financial support and making social distancing more feasible.

“It’s not rocket science. It’s not that we need some new thing that hasn’t been thought of before,” Jen Kates, director of global health and HIV policy at the Kaiser Family Foundation, told me. “There are things that have been done in some cases, or can be done. But if there was a stronger, coordinated federal role … that could really make a difference. It’s happened in other countries.”

Another part of Biden’s job will be to, in effect, repair Americans’ trust in science — bolstering public health institutions like the Centers for Disease Control and Prevention (CDC) and the Food and Drug Administration (FDA), widely considered the gold standard of public health agencies in the world before the pandemic.

Biden will also have to prepare the country for the rollout of a coronavirus vaccine that could take months if not years. The challenge here isn’t just discovering a safe and effective vaccine; many experts, in fact, are hopeful the world will do that by the end of 2020. The difficulty will be figuring out how to quickly produce and distribute up to hundreds of millions of doses of the vaccine to the general public — an unprecedented effort. That will also require persuading the public to take the vaccine, which could be particularly challenging coming off the heels of a highly contentious presidential election.

Biden, for his part, has vowed to do much of this. His website promises to adopt a masking mandate and boost testing and tracing. His campaign has vowed to “listen to science” and “restore trust, transparency, common purpose, and accountability to our government.” And he’s promised to “plan for the effective, equitable distribution of treatments and vaccines.”

Trump could do all of this, too. But there’s very little faith among experts that Trump will change his current approach to the pandemic, especially if he wins reelection. Instead, he’ll likely continue doing what he’s done: deliberately downplaying the pandemic, demanding states reopen far too quickly, punting testing and tracing to local and state governments with more limited resources, mocking masking, and continuing to try to politicize the CDC and FDA.

That failed response helps explain the US’s current Covid-19 outbreak, leading the country to more than 200,000 deaths from the disease — by far the highest recorded death toll in the world. When controlling for population, the US hasn’t had the highest death rate for Covid-19, but it’s among the top 20 percent for developed nations, and has seven times the death rate as the median developed country. If the US had the same Covid-19 death rate as, say, Canada, more than 120,000 more Americans would likely be alive today.

That damage can’t be reversed. Those 200,000 deaths are on the US’s record forever. But Biden, at least, could take actions that would help prevent America’s outbreak from getting even worse.

1) Implement policies we know work: Testing, tracing, masks, and social distancing

There are problems in the world with really difficult or unknowable answers. That’s not as true for Covid-19: While there’s a lot about the coronavirus we’re still learning, there are many policy approaches that we know work and the US hasn’t really embraced. This is, then, more a matter of will than knowledge — which is something that Biden, especially if he has a sympathetic Democrat-controlled Congress, could address.

Testing is among those proven policy approaches. When paired with contact tracing, more testing can help public health officials detect outbreaks, get the infected to isolate and the infected’s close contacts to quarantine, and use broader public health measures as needed. This is an approach that has worked well in many other developed countries, from Germany to South Korea to New Zealand.

The US, however, has struggled to build up its testing capacity. It’s made big improvements since the start of the pandemic, but testing hasn’t increased above 1 million tests a day — far lower than experts say is needed, given the country’s large epidemic overall. As a result, the percentage of tests coming back positive, which experts use to measure testing capacity, stubbornly remains at 5 percent or more; it should be, experts suggest, far below 5 percent and preferably below even 3 percent. It can still take days to get test results back, and that can spike to weeks if demand, due to a new outbreak, is high.

According to experts, part of the problem is the US never fundamentally fixed supply line problems — with shortages popping up for swabs, reagents, testing kits, and other needed equipment throughout the pandemic. There was also an economic disincentive to building out capacity too much: If a lab, for example, massively scales up its coronavirus testing, but the pandemic is over in a few years, it will be left with a lot of infrastructure it doesn’t use or get revenue from, a huge money sink.

A Biden administration could address these problems, using the powers of the federal government to coordinate the supply line, maintain its stability, and guarantee that any businesses and organizations will be made whole for investments into coronavirus testing. To do all of that, the country needs a national plan — which it currently lacks.

There’s a chance the supply problem fixes itself. With the development and mass production of new antigen tests that don’t have to go through a lab and hospitals, Americans could get access to many more tests that also return results within minutes instead of hours or days. Compared to the hold-ups with the current PCR tests that go through labs or hospitals, it would be a welcome change.

Still, there would be remaining questions about how to deploy and distribute those new tests based on equity and need — questions that a national plan could address.

After that, the US would still face another problem: how to actually use those tests. That’s where contact tracing comes in, as “disease detectives” track down newly infected people and their close contacts to convince them to isolate and quarantine. Earlier this year, Crystal Watson, senior scholar at the Johns Hopkins Center for Health Security, projected that the US would need at least 100,000 contact tracers. She estimated the US still has fewer than half of that number.

Since Watson’s original estimate, Covid-19 outbreaks in the US have also gotten much worse and more widespread. That presents two major problems: First, the US now needs even more contact tracers than she originally estimated. Second, it’s now likely impossible for contact tracing to really bring down the epidemic on its own, because there are just way too many cases for even a massive team of tracers to track down and contain.

So while a large federal investment in a contact tracing workforce and equipment could help, it probably won’t be enough. “We really have to take other measures to bring down transmission in order for contact tracing to be effective,” Watson told me.

Among the other measures: masks. The scientific evidence for masking has gotten much stronger since the start of the coronavirus pandemic, with multiple studies linking the widespread use of masks and new mask mandates to drops in Covid-19 cases and deaths. One study in Health Affairs suggested that, with caveats that this is just an approximation, “230,000-450,000 COVID-19 cases may have been averted on the basis of when states passed these mandates.” If mandates were nationwide instead of left to a minority of states at the time, it stands to reason the impact would have been much bigger.

Whether the federal government could impose a mask mandate on its own gets into legally dicey territory. But a Biden administration and Congress could use financial incentives to encourage cities and states to adopt masking mandates and provide extra resources to enforce them. That could get the remaining 16 states without a mask mandate, or at least some of the municipalities in those states, to adopt the policy.

Just having a president who is unequivocal about the benefits of masking and consistently wears a mask in public, experts claimed, would also signal to the rest of the country that this is the right thing to do. It’s “just the public image of a responsible adult doing what they’re supposed to do,” Cedric Dark, an emergency medicine physician at the Baylor College of Medicine, told me.

Even with all these measures in place, the US will have to continue social distancing to some degree. No one wants this, but, depending on how bad fall and winter outbreaks get, some cities, counties, and states may have to bring back lockdowns.

The federal government can provide clearer guidance on how and when to do this. It can also, with Congress’s backing, pass legislation that financially supports people affected by lockdowns. A commonly cited idea is a bailout for bars, restaurants, and other businesses, which would not only help keep these employers and their employees afloat but make the negatives of closing down much more tolerable and, therefore, make closing down easier and more likely if it’s deemed necessary to fight the coronavirus.

Ultimately, this could benefit the economy by mitigating the need for such harsh social distancing efforts. A preliminary study from the 1918 flu pandemic found that cities that took more aggressive action against outbreaks back then emerged stronger economically. Germany and others have similarly seen their restaurant businesses recover by controlling the coronavirus. As Watson put it, “In order for our economy to recover, we really do need to resource our public health response more effectively.”

Again, none of this is really new. The experts I spoke with often joked that we were having the exact same conversations now that we had back in the spring and summer. But the US hasn’t fully committed to these kinds of policies — and a Biden administration could.

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2) Rebuild trust in science and public health institutions

Under Trump, and particularly throughout this pandemic, trust in many institutions has dwindled. This has applied even to American institutions that were in the past considered the best of the best in the world for public health, such as the CDC and FDA.

The country needs “a long campaign to get people to trust science again,” Dark said. “My colleagues don’t trust anything coming out of the CDC now, due to how politicized it’s been.”

A report from the Covid-19 Consortium for Understanding the Public’s Policy Preferences Across States, based on a 50-state survey on Covid-19, captured the trends: Across the country, trust in “doctors and hospitals,” “scientists and researchers,” and especially the CDC has fallen. Trust in all of these is still relatively high — much higher than trust in either Biden or Trump — but it’s a concerning trend. Among different political and demographic groups, trust can be even lower, too.

“Six months ago, the FDA and CDC were shorthands for gold-standard scientific advice,” Ashish Jha, dean of the Brown University School of Public Health, told me. That’s changed, he lamented.

Some of this reflects genuine failures by these institutions. The CDC and FDA both played roles in the US’s testing problems — the CDC by botching its tests, and the FDA dragging its feet in approving more testing from private and independent labs — leading to what’s been widely called a “lost month” for testing in February. The CDC was also slow to recommend masks, then failed to admit to messing up and explain its about-face on the issue. The FDA, meanwhile, has acted in ways that seem politically motivated rather than based on rigorous evidence, such as when it allowed, before warning against, hydroxychloroquine, which was always unproven but Trump spoke favorably about.

Although the CDC and FDA are supposed to stand above partisan politics to help maintain their credibility, Trump and his administration have actively meddled in their affairs and work. Trump and his political cronies have, for example, repeatedly pushed the CDC to do things solely to support Trump’s unproven claims about Covid-19 — forcing the agency to briefly recommend less testing, loosen its guidelines for reopening, and delay studies that contradict the president. All of that has called into question just how independent the CDC truly is.

Fixing this will take time, but it’s fairly straightforward: Biden and the political actors in his administration should back off, allowing scientists to take a leading role in these agencies and the US’s Covid-19 response in general.

Carlos del Rio, executive associate dean of the Emory University School of Medicine, put this simply: “Pay attention to science. Let the science guide the response, not the politics.”

That includes giving these institutions control of the public messaging. While Trump appointed Vice President Mike Pence to lead the White House’s coronavirus task force, Biden could put a scientist or public health official in charge. While Trump sidelined the CDC after Nancy Messonnier, director of the CDC’s National Center for Immunization and Respiratory Diseases, warned in February that “disruption to everyday life might be severe” due to Covid-19, Biden could allow the agency and its experts to speak plainly and truthfully to the public.

That should also translate to the policy level. When the CDC makes recommendations, the Biden administration shouldn’t, as Trump has, undermine the guidelines or force the agency to change them. When scientists are recommending a pivot in the country’s approach, that should be seriously considered, even if it contradicts what the administration said or did in the past, while clearly and transparently explaining why a change is needed.

“The CDC has the expertise to lead us in this pandemic,” Jorge Salinas, an epidemiologist at the University of Iowa, told me. “We just need to ask them.”

The idea is to prove to the public time and time again that the country’s response to Covid-19 isn’t driven by politics but by science. It’s an admittedly difficult task for a country that’s consumed by politics and polarization at every level, but it’s something, experts said, that’s simply necessary to improve America’s response to the coronavirus.

3) Prepare the country for a months-long rollout of a vaccine

If we get a little lucky, there’s a chance that the world will finally have a proven, safe, and effective coronavirus vaccine by the end of the year. It would be an incredible achievement — the fastest turnaround on a vaccine for a major disease in human history.

But that won’t be the end. After a vaccine makes it through the last rounds of research necessary to get FDA approval, it’ll have to be distributed to potentially more than 300 million people in the US alone. Given that some of these vaccines will require two doses, that means manufacturing hundreds of millions of doses of the medication — something that the country simply hasn’t done at the scale and speed that the pandemic demands.

There’s already a lot of work, from both governments and private actors like Bill Gates, to manufacture all those doses. It’s possible, even likely, that the current work isn’t enough — and that will demand more action and more funds by a Biden administration.

After that, there will be tough questions about who gets priority. There’s a consensus that first responders and health care workers, at least, should get a vaccine first. Beyond that, there are genuinely difficult questions: Should older adults get priority because they’re more vulnerable? Should essential workers? What about younger people, who seem to be behind the country’s most recent large outbreaks? “It gets complicated,” Jha acknowledged.

Another element will be persuading the public to actually take a vaccine. If a vaccine is 50 to 70 percent effective, as appears likely at first, experts argue that close to 100 percent of the population will need to take one to reach true herd immunity. That will be a tall order as the country deals not just with traditional, unscientific anti-vaxxer sentiments but also more nuanced concerns about whether the current politicized, fast process coronavirus vaccines are going through can really test adequately for safety. Different surveys have found a third to half of Americans don’t plan to or don’t know if they’ll get a coronavirus vaccine.

“It does seem like there has been less of a push to actually come up with a really good communications plan,” Watson said, “but also to just have a general dialogue with people as you go along about what the process has been like for creating a vaccine, what standards have been upheld, and the results of the safety and efficacy trials.”

Breaking through those concerns will require research and surveys to subsequently build a massive communications campaign that will try to push people to get vaccinated. This will be a huge undertaking, and it might not even work, depending on if a new administration can rebuild trust in science and depoliticize its public health institutions.

All of this could take a long time. Experts were unanimous in arguing that getting a vaccine by the end of 2020, should that happen, won’t be the end of the pandemic. They said that getting a vaccine out there could take at least months. Some spoke in terms of years, well into 2022 or 2023. “President Biden and Vice President [Kamala] Harris, should they be in office, should understand they will be dealing with Covid for much of their first term,” Jha said. “It will continue to come up as an issue in the next midterms. It’s not going away.”

To put it another way: If Biden takes office, it’s possible a vaccine will finally present some kind of finish line in this pandemic. But we might quickly realize that the finish line is still a few months or years away. And that will make the work of preparing the country for a vaccine — and all the other steps needed to contain Covid-19 in the months and years ahead — necessary. With hundreds of thousands of Americans already dead, it’s the most important task Biden should prepare for right now.

Mushrooms that don’t brown. A treatment for sickle-cell anemia. Driving malaria-carrying mosquitoes to extinction. Resurrecting the woolly mammoth. Editing genes in human embryos to make them less susceptible to HIV. These are just a handful of the possibilities of the versatile gene editing tool known as CRISPR that scientists have explored in the few years since its discovery.

On Wednesday, the 2020 Nobel Prize in chemistry was awarded to the pair of scientists who discovered the CRISPR gene-editing mechanism, also known as CRISPR/Cas9. It acts as a pair of “genetic scissors” to precisely make cuts and insertions in genomes, creating the possibilities of treating genetic maladies, as well as introducing new heritable traits into living organisms.

Emmanuelle Charpentier, director of the Max Planck Unit for the Science of Pathogens in Berlin, Germany, and Jennifer Doudna, a professor at the University of California, Berkeley, will split the $1.1 million prize evenly, marking the first time two women scientists have been awarded the chemistry Nobel without a male collaborator.

“This year’s prize is about rewriting the code of life,” Göran K. Hansson, Secretary General of the Royal Swedish Academy of Sciences said on Wednesday.

It’s hard to overstate the impact of Charpentier and Doudna’s discovery. In 2011, there were fewer than 100 published papers on CRISPR. In 2020, there were more than 35,000. Dozens of companies have sprung up to develop products from this technique, from therapies for genetic diseases to engineered crops. Scientists have even developed a CRISPR-based test to detect SARS-CoV-2, the virus that causes Covid-19.

All this from an ancient defense mechanism found in common bacteria.

The CRISPR/Cas9 technique has managed to simultaneously improve the precision and speed of genome editing, while also lowering the cost of this manipulation. Despite all the progress to date, there may be many more discoveries built on this foundation that lie ahead.

With the Covid-19 pandemic raging around the world, Charpentier and Doudna will not be able to accept their prizes in person this year and will instead participate in a digital ceremony in December. “I can guarantee you that Doctors Charpentier and Doudna will receive their awards before the end of the year, and that they will be our guests of honor next time we can celebrate Nobel week with the traditional festivities here in Stockholm,” Hansson said.

How CRISPR sequences and the Cas9 enzyme work to edit genomes

The roots of the discovery date back to 1987, when Japanese researchers looking at E. coli found a strange section of DNA in the bacteria. There were short, repeating clusters of the DNA sequence that could be read in the same way forward and backward, forming palindromes.

They named these sequences Clustered Regularly Interspaced Short Palindromic Repeats, or CRISPR, but the scientists at the time didn’t know what purpose they served.

Then in 2007, researchers studying the Streptococcus bacteria used to make yogurt discovered these sequences are part of how bacteria resist infections from viruses.

When a bacterium fights off a virus, it keeps a small section of the virus’ genetic material as a souvenir, storing the information from the fragment in the spaces between CRISPR segments in its own genome.

If a similar virus attacks again, the bacteria produces an enzyme called Cas9. It uses the stored bits of viral genetic material in CRISPR spaces as sort of a mugshot. When it identifies a matching strand, it cuts it into pieces. This thwarts a virus from replicating.

In 2011, Charpentier and Doudna figured out that they could replace the template that Cas9 uses to snip genetic material with a synthetic code of their choosing. The enzyme then would search for a match to the new template and cut that out instead. This demonstrated that they could harness this mechanism to make cuts in a genome at any place they wanted.

The researchers published their findings in a 2012 paper in the journal Science.

The science of gene editing is advancing much faster than the ethics

While genetic-editing techniques have been around for decades, the CRISPR/Cas9 system introduced a new level of precision. It’s also fast and cheap, condensing genetic manipulation that previously took months and cost thousands of dollars into a system that can work in hours from a kit that you can buy online for less than $200 (“you don’t need anything else but water and a microwave,” it advertises).

The potentially lucrative applications of CRISPR/Cas9 have fueled an ongoing patent dispute between a team at the Broad Institute led by Feng Zhang and Doudna’s team at Berkeley. In 2013, Zhang, showed in a paper in Science that CRISPR/Cas9 could be used to edit the genomes of cultured mouse cells or human cells.

The growing use of such a sophisticated genetic manipulation tool has also proven controversial, especially as a small number of scientists have pushed forward with using it in human embryos despite an international consensus that it was too soon (outside of a serious medical need). In 2018, He Jiankui, a researcher in China, announced that he had already used CRISPR to edit the genomes of the embryos of a pair of twin girls, marking the first time human embryos have been genetically edited.

The story generated international outcry and calls for stricter regulations on using this kind of genetic manipulation. He was later sentenced to three years in prison by Chinese authorities for forging ethics review documents and misleading the doctors involved about the nature of his experiment.

In a 2018 statement responding to He’s announcement, Doudna called for constraints on how CRISPR is used in humans. “The work as described to date reinforces the urgent need to confine the use of gene editing in human embryos to cases where a clear unmet medical need exists, and where no other medical approach is a viable option, as recommended by the National Academy of Sciences,” she wrote.

The National Academy of Sciences in September put out a report assessing the state of genetic manipulation and concluded that such techniques are still not ready for use in humans.

“No attempt to establish a pregnancy with a human embryo that has undergone genome editing should proceed unless and until it has been clearly established that it is possible to efficiently and reliably make precise genomic changes without undesired changes in human embryos,” according to the report. “These criteria have not yet been met and further research and review would be necessary to meet them.”

Further reading about the 2020 Nobel Prizes:

• Andrea Ghez and Reinhard Genzel shared the Nobel Prize in physics for leading teams who made revolutionary observations of black holes.
• Harvey J. Alter, Michael Houghton, and Charles M. Rice shared the Nobel Prize in medicine for discovering hepatitis C.

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Researchers at the University of Nevada have reported that a 25-year-old man was reinfected in June with SARS-CoV-2, the virus the causes Covid-19. He joins a handful of other confirmed cases of reinfection in people without immune disorders — in Belgium, the Netherlands, Hong Kong, and Ecuador — where researchers have demonstrated that the genetic signature of the second infection did not match that of the first.

According to a new study on the Nevada case, published in The Lancet Infectious Diseases journal, the patient first tested positive in April, and then tested negative for the virus twice. In June, 48 days later, “the patient was hospitalized and tested positive for a second time,” according to the authors, and he experienced severe symptoms. There were major genetic differences between the two infections, suggesting that the patient got the virus twice. (Since then, the patient has recovered.)

The report is in line with what immunity experts have been telling us is possible with this virus: that reinfection is possible and, to some extent, expected, with a coronavirus. But it also shows us how much we still have to learn: about how much protection a single infection can confer, about what exactly a robust long-duration immune response looks like, and about what determines the severity of disease in a second infection.

“Does immunity protect an individual from disease on reinfection?” writes Yale immunobiology researcher Akiko Iwasaki in an accompanying editorial in The Lancet Infectious Diseases. “The answer is not necessarily, because patients from Nevada and Ecuador had worse disease outcomes at reinfection than at first infection.”

The Nevada case is an important finding, since in the two other confirmed cases of reinfection, the patients had mild disease or were asymptomatic. Scientists still don’t know how common reinfection is (it may well be very rare), nor can they determine an individual’s chances of getting infected again.

They do know there are many, many components of our immune system that work together to fight the coronavirus, and immunity doesn’t mean one single thing. And while we’re waiting for scientists to figure it all out, everyone, including those who’ve already had the virus, should still try to avoid getting infected at all.

The new study “strongly suggests that individuals who have tested positive for SARS-CoV-2 should continue to take serious precautions when it comes to the virus, including social distancing, wearing face masks, and handwashing,” said Mark Pandori, of the Nevada State Public Health Laboratory at the University of Nevada Reno School of Medicine and lead author of the study, in a statement.

Let’s walk through the basics of immunity, and what we’re learning about reinfection.

There are no simple stories about immunity and Covid-19

The immune system is profoundly complicated, and “immunity” can mean many different things. A lot of this nuance gets lost in headlines about immunity.

For instance: Previous research has shown that neutralizing antibodies — immune system proteins that latch onto pathogens and prevent them from infecting cells — can wane in the months after a Covid-19 infection, particularly when the initial infection was mild. Some wondered if that meant the end of herd immunity hopes.

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In the Nevada case, we know that “the patient had positive antibodies after the reinfection, but whether he had pre-existing antibody after the first infection is unknown,” writes Iwasaki.

But what’s often misunderstood is that antibodies are only one component of the immune system, and losing them does not leave a person completely vulnerable to the virus.

In fact, there are several parts of the immune system that may contribute to lasting protection against SARS-CoV-2.

One is killer T-cells. “Their names give you a good hint what they do,” Alessandro Sette, an immunologist at the La Jolla Institute for Immunology, told me in July. “They see and destroy and kill infected cells.”

Antibodies, he explained, can clear virus from bodily fluids. “But if the virus gets inside the cell, then it becomes invisible to the antibody.” That’s where killer T-cells come in: They find and destroy these hidden viruses.

While antibodies can prevent an infection, killer T-cells deal with an infection that’s already underway. So they play a huge role in long-term immunity, stopping infections before they have time to get a person very sick.

And it’s not just killer T-cells and antibodies. There are also helper T-cells, which facilitate a robust antibody cell response. “They are required for the antibody response to mature,” Sette says.

Some proportion of the population (perhaps 25 to 50 percent of people) seems to have some preexisting T-cells (of both varieties, but the helper kind have been more commonly observed) that respond to SARS-CoV-2, despite these people never having been exposed to SARS-CoV-2. The hypothesis is that these people may have acquired these T-cells from being infected with other strains in the coronavirus family of viruses. Researchers still don’t really understand what role these preexisting T-cells play in preventing or attenuating infection (if any).

But wait, there’s more! There’s another group of cells called memory B-cells. B-cells are the immune system cells that create antibodies. Certain types of B-cells become memory B-cells. These save the instructions for producing a particular antibody, but they aren’t active. Instead, they hide out — in your spleen, in your lymph nodes, perhaps at the original site of your infection — waiting for a signal to start producing antibodies again.

All the things “immunity” can mean

All these different components of the immune system mean “immunity” isn’t just one thing.

Immunity could mean a strong antibody response, which prevents the virus from establishing itself in cells. But it could also mean a good killer T-cell response, which could potentially stop an infection very quickly: before you feel sick and before you start spreading the virus to others.

“In many infections, the virus does reproduce a little bit, but then the immune response stops this infection in its tracks,” Sette explains. Also possible: “You do get infected, you do get sick, but your immune system does enough of a job curbing the infection, so you don’t get as sick.”

Immunity might also result from an awakening of memory B-cells. If an individual has memory B-cells and is exposed to the virus again, “that infection will stimulate a much faster antibody response to the virus, which would, theoretically lead to faster clearance of the virus and potentially less severe infection,” Elitza Theel, the director of the infectious diseases serology laboratory at the Mayo Clinic, said in a July interview.

In general, scientists believe, the stronger the infection (and immune response) that occurs during an initial infection, the longer immunity will last.

So reinfection may still be possible, but it may not mean severe illness. When a virus invades a body, generally, the body remembers.

Could asymptomatic infections spread the virus? Unclear.

It’s still not known what the latest reinfection study means for how long the pandemic will last. If reinfections happen regularly (and we have no idea how common they might be), then it might take longer to achieve herd immunity without a vaccination (which is an un-ideal, and cynical, goal to begin with). How long immunity lasts, on average, and how common reinfection is are key unknown variables in figuring out how long the pandemic may last in the absence of an effective vaccine or treatment.

“Reinfection cases tell us that we cannot rely on immunity acquired by natural infection to confer herd immunity; not only is this strategy lethal for many but also it is not effective,” Iwasaki wrote in the editorial. “Herd immunity requires safe and effective vaccines and robust vaccination implementation.”

We also have much more to learn about how often reinfections lead to more clusters of cases. Recently, I asked Shane Crotty, an immunologist at the La Jolla Institute for Immunology, about this very scenario.

“Could there be an ‘immunity’ scenario,” I asked, “where, after having recovered from Covid, a person could get infected again but not feel sick at all, and also be able to spread it?”

“It is a good question, and the answer is that no one knows,” Crotty replied. “There are cases with other diseases where asymptomatic immune people can be infectious. There is definitely a lot to learn still about immunity to SARS-CoV-2.”

Much ink has been spilled over the “replication crisis” in the last decade and a half, including here at Vox. Researchers have discovered, over and over, that lots of findings in fields like psychology, sociology, medicine, and economics don’t hold up when other researchers try to replicate them.

This conversation was fueled in part by John Ioannidis’s 2005 article “Why Most Published Research Findings Are False” and by the controversy around a 2011 paper that used then-standard statistical methods to find that people have precognition. But since then, many researchers have explored the replication crisis from different angles. Why are research findings so often unreliable? Is the problem just that we test for “statistical significance” — the likelihood that similarly strong results could have occurred by chance — in a nuance-free way? Is it that null results (that is, when a study finds no detectable effects) are ignored while positive ones make it into journals?

A recent write-up by Alvaro de Menard, a participant in the Defense Advanced Research Project’s Agency’s (DARPA) replication markets project (more on this below), makes the case for a more depressing view: The processes that lead to unreliable research findings are routine, well understood, predictable, and in principle pretty easy to avoid. And yet, he argues, we’re still not improving the quality and rigor of social science research.

While other researchers I spoke with pushed back on parts of Menard’s pessimistic take, they do agree on something: a decade of talking about the replication crisis hasn’t translated into a scientific process that’s much less vulnerable to it. Bad science is still frequently published, including in top journals — and that needs to change.

Most papers fail to replicate for totally predictable reasons

Let’s take a step back and explain what people mean when they refer to the “replication crisis” in scientific research.

When research papers are published, they describe their methodology, so other researchers can copy it (or vary it) and build on the original research. When another research team tries to conduct a study based on the original to see if they find the same result, that’s an attempted replication. (Often the focus is not just on doing the exact same thing, but approaching the same question with a larger sample and preregistered design.) If they find the same result, that’s a successful replication, and evidence that the original researchers were on to something. But when the attempted replication finds different or no results, that often suggests that the original research finding was spurious.

In an attempt to test just how rigorous scientific research is, some researchers have undertaken the task of replicating research that’s been published in a whole range of fields. And as more and more of those attempted replications have come back, the results have been striking — it is not uncommon to find that many, many published studies cannot be replicated.

One 2015 attempt to reproduce 100 psychology studies was able to replicate only 39 of them. A big international effort in 2018 to reproduce prominent studies found that 14 of the 28 replicated, and an attempt to replicate studies from top journals Nature and Science found that 13 of the 21 results looked at could be reproduced.

The replication crisis has led a few researchers to ask: Is there a way to guess if a paper will replicate? A growing body of research has found that guessing which papers will hold up and which won’t is often just a matter of looking at the same simple, straightforward factors.

A 2019 paper by Adam Altmejd, Anna Dreber, and others identifies some simple factors that are highly predictive: Did the study have a reasonable sample size? Did the researchers squeeze out a result barely below the significance threshold of p = 0.05? (A paper can often claim a “significant” result if this “p” threshold is met, and many use various statistical tricks to push their paper across that line.) Did the study find an effect across the whole study population, or an “interaction effect” (such as an effect only in a smaller segment of the population) that is much less likely to replicate?

Menard argues that the problem is not so complicated. “Predicting replication is easy,” he said. “There’s no need for a deep dive into the statistical methodology or a rigorous examination of the data, no need to scrutinize esoteric theories for subtle errors — these papers have obvious, surface-level problems.”

A 2018 study published in Nature had scientists place bets on which of a pool of social science studies would replicate. They found that the predictions by scientists in this betting market were highly accurate at estimating which papers would replicate.

“These results suggest something systematic about papers that fail to replicate,” study co-author Anna Dreber argued after the study was released.

Additional research has established that you don’t even need to poll experts in a field to guess which of its studies will hold up to scrutiny. A study published in August had participants read psychology papers and predict whether they would replicate. “Laypeople without a professional background in the social sciences are able to predict the replicability of social-science studies with above-chance accuracy,” the study concluded, “on the basis of nothing more than simple verbal study descriptions.”

The laypeople were not as accurate in their predictions as the scientists in the Nature study, but the fact they were still able to predict many failed replications suggests that many of them have flaws that even a layperson can notice.

Bad science can still be published in prestigious journals and be widely cited

Publication of a peer-reviewed paper is not the final step of the scientific process. After a paper is published, other research might cite it — spreading any misconceptions or errors in the original paper. But research has established that scientists have good instincts for whether a paper will replicate or not. So, do scientists avoid citing papers that are unlikely to replicate?

This striking chart from a 2020 study by Yang Yang, Wu Youyou, and Brian Uzzi at Northwestern University illustrates their finding that actually, there is no correlation at all between whether a study will replicate and how often it is cited. “Failed papers circulate through the literature as quickly as replicating papers,” they argue.

Looking at a sample of studies from 2009 to 2017 that have since been subject to attempted replications, the researchers find that studies have about the same number of citations regardless of whether they replicated.

If scientists are pretty good at predicting whether a paper replicates, how can it be the case that they are as likely to cite a bad paper as a good one? Menard theorizes that many scientists don’t thoroughly check — or even read — papers once published, expecting that if they’re peer-reviewed, they’re fine. Bad papers are published by a peer-review process that is not adequate to catch them — and once they’re published, they are not penalized for being bad papers.

The debate over whether we’re making any progress

Here at Vox, we’ve written about how the replication crisis can guide us to do better science. And yet blatantly shoddy work is still being published in peer-reviewed journals despite errors that a layperson can see.

In many cases, journals effectively aren’t held accountable for bad papers — many, like The Lancet, have retained their prestige even after a long string of embarrassing public incidents where they published research that turned out fraudulent or nonsensical. (The Lancet said recently that, after a study on Covid-19 and hydroxychloroquine this spring was retracted after questions were raised about the data source, the journal would change its data-sharing practices.)

Even outright frauds often take a very long time to be repudiated, with some universities and journals dragging their feet and declining to investigate widespread misconduct.

That’s discouraging and infuriating. It suggests that the replication crisis isn’t one specific methodological reevaluation, but a symptom of a scientific system that needs rethinking on many levels. We can’t just teach scientists how to write better papers. We also need to change the fact that those better papers aren’t cited more often than bad papers; that bad papers are almost never retracted even when their errors are visible to lay readers; and that there are no consequences for bad research.

In some ways, the culture of academia actively selects for bad research. Pressure to publish lots of papers favors those who can put them together quickly — and one way to be quick is to be willing to cut corners. “Over time, the most successful people will be those who can best exploit the system,” Paul Smaldino, a cognitive science professor at the University of California Merced, told my colleague Brian Resnick.

So we have a system whose incentives keep pushing bad research even as we understand more about what makes for good research.