Category Archives: Corona Virus

A transmission-electron micrograph of SARS-CoV-2 Omicron virus particles (pink) replicating within the cytoplasm of an infected CCL-81 cell (teal). Photo: NIAID Integrated Research Facility/NIAD

Were still in the midst of one of the largest COVID waves of the pandemic, and its fueled by the Omicron BA.5 subvariant, the most contagious and most immune-evasive coronavirus strain yet. Scrippss Dr. Eric Topol, who has been one of the loudest voices sounding the alarm over BA.5, has repeatedly described the strain as the worst COVID variant on account of it having more fitness, growth advantage, and immune evasion than any of its predecessors. According to the latest CDC estimate, BA.5 now accounts for nearly 82 percent of all new infections in the U.S., where it has prompted a surge in reported cases, test-positivity rates, COVID wastewater levels, and, thanks to its immune evasion, reinfections. Last week, it even infected President Biden with his first-ever COVID case; this week, an outbreak hit the Senate.

The BA.5 wave has also been driving up the number of U.S. hospitalizations, along with a slight rise in the number of COVID deaths, but it hasnt produced severe outcomes anywhere near the scale seen in previous major waves. Indeed, the rapid onset of BA.5 and its subvariant brethren (BA.4, BA.2, and BA.2.12.1) without a corresponding surge in severe COVID has prompted a sense that were finally in a new phase of the pandemic where new strains come and go, COVID continues to spread and surge and unsettle, but our bolstered immune systems hold the line and we avoid the recurring nightmare of mass illness and death.

Scientists are still studying the new variant, and the BA.5 wave has been playing out differently in various countries, likely due to a complicated combination of factors. But while the far less severe impact of the BA.5 wave in the U.S. has, thus far, been a welcome departure from what weve encountered before, some COVID experts, like Topol, remain concerned. Though its been more than two and a half years since COVID arrived, were still not staying ahead of the virus.

Topol and immunologist Akiko Iwasaki just co-wrote a paper calling for an accelerated Operation Warp Speedlike initiative to pursue nasal COVID vaccines, which could provide mucosal immunity that stops the virus in the part of the body where it starts. Topol has also pushed for the development of other potentially variantproof vaccines, like pan-sarbecovirus and pan-coronavirus vaccines. This week, the White House hosted a summit on future COVID vaccines attended by many of the top minds in the field, including Iwasaki, but its far from clear that any of the promising ideas and goals discussed there will get the government funding theyd need to have an impact on the pandemic anytime soon.

I recently had a long conversation with Topol about BA.5, why hes troubled by it, and what the variant and its arrival portend for the future.

On one hand, here in the U.S. weve seen a significant drop in hospitalizations and deaths amid the wave of cases of BA.5 and the other earlier Omicron subvariants. But youve been calling attention to the fact that in some other countries, BA.5 has fueled some alarming spikes in cases, hospitalizations, and even deaths. So, is the U.S. through the worst of this?I agree that, overall, if you look at it globally, hospitalizations and deaths from BA.5 are not going to reach levels anywhere close to Omicron or previous waves, but theyre not trivial elevations. Deaths are going up over the whole world from BA.5. Our wave is still playing out right now. Were poorly vaccinated here in the U.S. poorly boosted, especially in high-risk people like seniors. So I wouldnt want to conclude that were out of the woods. We could be in for more trouble before the BA.5 wave is finished.

Im actually a very optimistic person. When we were coming down from Delta and had not seen Omicron, I thought, Wow, the worst is over. Then Omicron proved to be an onslaught in terms of spread by any metric as well as the toll it took in more serious outcomes. So with that background, the recent CDC report that came out about the vaccines really has me worried.

Whys that?Its not like all of a sudden theres going to be a variant with total immune escape from vaccines. But in the CDC morbidity and mortality report, it said that two-dose vaccine effectiveness against hospitalization for the original BA.1 Omicron strain were not talking about infections because were well past having good vaccine coverage for that but for hospitalization, it dropped to 61 percent for two doses. And for BA.2 and BA.2.12.1, the latter of which is more like BA.5 but not as bad, two doses against hospitalization dropped to 24 percent. That should set off alarms because we dont have a lot of people with a third shot. For three shots the efficacy jumped back up, but only to 52 to 69 percent with BA.2/2.12.1.

Kaiser Southern California has also had two reports on vaccine effectiveness in their big network of patients, and they show the same attrition against hospitalizations as was seen in this much larger new comparison from the CDC.

So how can you feel good about these data? I dont see how. This narrowing benefit of the vaccines, which I think is due to more immune escape, not due to more infections in the unvaccinated, its still a very big gap. To drop down almost 40 points in effectiveness against hospitalizations with only two shots this should be a signal that something is going on with our vaccine protection. But you dont see anybody raising concerns about this. All you hear is happy talk that we have great protection from hospitalizations and deaths. I dont know about that. These data dont support that.

So that suggests that hospitalizations will likely keep going up in the BA.5 wave? Yeah, theyre going to go up. The number of current U.S. hospitalizations is already over 40,000. I wouldnt be surprised if it gets to 50,000 or 60,000. It isnt going to get near 160,000, like it did with BA.1, only because so many people got infected with BA.1 and theres some cross-immunity. But the number of hospitalizations has been going up substantially. It had gotten down to 12,000 and now back up past 40,000. If you look at the curve, it has a new increased slope since BA.5 started to take effect, and its still on the way up. The question is does it get to 50,000? Does it get to 60,000? Thats a lot of sick people in the hospital.

And the other thing I would just say, parenthetically, is with BA.5, Ive never seen so many infections in my personal network, including family, friends, colleagues. Ive never seen infections last as long. After 10 days, still testing positive, after day 12, 13, 14. The behavior of BA.5 is different and the fact that our CDC still adheres to this five-day isolation recommendation, its incredulous. Theyre actually promoting spread by doing that.

Theres no question that this is a different effect from BA.5 in terms of the length of infectiousness, how much its spread, and maybe not more hospitalizations. But remember, thats with Paxlovid, which now has 90 percent efficacy in preventing hospitalizations for high-risk people.

Right, if a variant emerges that Paxlovid isnt as effective against, that could suddenly leave us much more vulnerable to severe COVID again.Yes. And I think most of us whove really zoomed into the mutations on MPro, the main protease of the virus that Paxlovid works on Id say its just a matter of time. Its inevitable. Already these mutations have appeared naturally because of the pressure that the virus is getting from Paxlovid. Its inevitable. Were going to see resistance to this drug, which, after the vaccines, is the second-most-important advance that we have had to take on the virus. But it may be short-lived, it could be that by years end or the beginning of next year, we wont have Paxlovid as a remedy or rescue anymore. Theres no question Paxlovid is helping keep the hospitalization number down.

Updated booster shots that better target the Omicron lineage are on the way. Will those help us stay ahead of the virus?We need variantproof boosters. No more chasing variants because we are not very good at that. Just get the vaccines that would take on all sarbecovirus and betacoronavirus so we can put an end to the whole idea of trying to anticipate the variant that well need a booster for. We know how to do that. We have over 25 incredibly potent broad neutralizing antibodies. We can make vaccines that induce several of those antibodies to never have to worry about a variant in terms of having protection.

But those arent the boosters arriving this fall.No. The booster plan is for BA.5. And saying that will be here for the fall is highly optimistic. It took seven months to get a BA.1 booster. Then the government sent the pharmaceutical companies back to go get us a BA.5 booster. Thinking that could be available in October or November thats highly optimistic. And we certainly dont know what variant is going to be with us at that time. It wont be BA.5 anymore. Therell be something else that will outcompete BA.5. Once that BA.5 booster is available, it may not work against the then circulating virus because it knows how to evolve.

Why arent these better boosters in the pipeline instead?Well, its pretty clear that Congress is unwilling to fund a dollar more for COVID. And thats, of course, the Republicans blocking any COVID bill. But there are even people in the Biden administration who arent sure how much these next-generation vaccines including variantproof, universal, and nasal are going to help us. Thats just, I think, being out of touch with the science. And any COVID bill dedicated to getting ahead of the virus would need to include better drugs, more drugs. Because we have to plan for Paxlovids obsolescence, and we dont have anything to replace it yet but there are many good candidates in the pipeline.

There seems to be at least anecdotal evidence that a small number of people are now getting reinfected within a matter of weeks. What do you make of that?Those added mutations that we first saw with BA.2.12.1 and now in BA.4 and BA.5 that immune evasion is whats responsible for all these early reinfections. Thats where this virus is going. Its got a flashing light: I have found ways to evade your immune system, and I can keep building on that. Reinfection is perhaps the best real-time signature of immune evasion.

Whats your sense of where long COVID is going? Is there any other way to avoid it than just not catching regular COVID in the first place, which is clearly getting harder to do at this point in the pandemic? Is there some other way to handle it?Well, youre right. Avoid the infection, first. Then, if you had a vaccine, that seems to avoid the chance of long COVID to some extent, but we also have to have treatments for it we dont have any yet that are validated. We have a billion dollars from the NIH toward long COVID, but youre not seeing any real contributions that funding has advanced yet. And we know that long COVID is not a homogeneous disorder. There are different components. Some are much more immune-mediated, some are much more autonomic nervous system-mediated. So theres a lot to unpack with that.

So what are you most worried about with regard to the future evolution of SARS-CoV-2?The known unknown, which is that this virus still has many more ways to become more resistant to our immune response and we should plan on that. We keep thinking weve reached some kind of limit. But the most important lesson from BA.5, to me, is that its worse. If it had come without BA.1 as a predecessor the only reason BA.5 doesnt look horrific right now is because BA.1 had built up the immunity wall. More than half of Americans have had BA.1 or BA.2. And were now seeing in BA.5 the most innovation, the most growth advantage, the most fitness of the virus yet and were just not dealing with it.

If some people think, Oh, it cant get worse, its going to get better. We dont know that. You have to plan for the worst-case scenario. And the worst-case scenario is that the virus further increases its immune evasion. Its already picking up things that worked in prior versions of the virus: For instance, BA.2.12.1 and BA.5 have the same key L452R mutation that the Delta variant had. Anyone who thinks the virus doesnt have room to evolve further is just not paying attention.

Is that a near-term threat? Can we predict a timetable for any of this evolution? No, but its accelerating. We know that much. The time its taken to get from BA.1 to BA.5 is not a good tempo for a whole new lineage to outcompete the prior one and achieve dominance worldwide.

So it doesnt look good. These new strains are clearly happening more frequently than they used to. In the first 12 months of the pandemic, there was no evolution of the virus. We basically had the original Wuhan strain, and then D614G, which arguably only had minor functional consequences. Alpha was mild compared to anything weve seen subsequently, then there was Delta, which obviously had more infectiousness and virulence. But now, with this whole Omicron family, its moving at a very rapid pace.

We cant predict the new mutations. We cant predict the timing. We can try to extrapolate, but even extrapolating, we had no good semblance of what Omicron would look like with its 57 spike mutations in BA.1. No one accurately predicted we would be looking at that.

And its too fast.Its the known unknown. Yeah.

UCL Genetics Institute director Francois Balloux recently explained that he wasnt as concerned about the emergence of further Omicron subvariants as he was about the reemergence of COVID lineages, like Delta, that have undergone a kind of underground evolution. So a strain circulating in some isolated part of the world; or one within an animal reservoir, i.e. an animal population the virus has spilled into from humans; or one that has evolved via a long-term chronic infection in someone who is immunocompromised which is how many scientists believe Omicron itself evolved. How worried are you about these paths?When an immunocompromised person gets infected, they really cant mount a good immune response. So the virus, instead of what its been doing globally for two and a half years, goes through this accelerated evolution in that person, picking up mutations left and right. It basically has unchecked potential to evolve in that person, and then that evolved virus infects other people. Thats pretty certainly what happened with Omicron.

I agree that the animal reservoirs are also a concern because weve already seen spillover to many different species, including hamsters, mink, cats, and deer. So thats another way that the virus can evolve, in an animal reservoir, and come back to spillover in humans.

We also havent contained the virus around the world, so it can continue to evolve through the millions of infections each day. And there are tens of millions of immunocompromised people in the world. It just takes one person, really, to trigger things. And then you have all these hybrid versions of the virus that were seeing, all these recombinants, which could bring about the worst elements of different parts of the virus. Most of the public focus on the evolution of SARS-CoV-2 has been spike-centric, but there are lots of other parts of the virus that can be troubling, that can make the virus more difficult to deal with. So again, theres lots of room for this virus to go.

There are too many paths. If youre just taking odds, and you have all these different routes and tens of millions of people that are immunocompromised around the world, are you going to bet against the virus evolving into something thats more challenging than what we have today? I dont think so.

Is there anything we can do to defend against COVID strains spilling back over from animal populations?No. No defense at all, unfortunately.

You and some other scientists have suggested that Omicron and particularly BA.5 are so different from any previously dominant COVID strains that in many ways we are now effectively dealing with a new virus. Youve also pointed out that if the original Omicron strain had the characteristics of BA.5,the Omicron wave would have been far worse. I understand thats a way to highlight why people should be concerned about BA.5 and what it means for COVIDs evolution, but is that actually possible? Can a BA.5 evolve on its own without there first having been a BA.1?Its a good question because we dont really know how BA.5 evolved. We just know it did. And could BA.5 have come in from an immunosuppressed person de novo without BA.1? Possibly. We just dont know. Basically new mutations showed up. Four key mutations showed up beyond BA.2 that have caused a lot of trouble, but we dont really know precisely how that occurred.

But we know why it occurred.Yeah. The virus is under pressure from vaccines and prior infections and now Paxlovid. So its finding ways to stand up to find new hosts. All viruses want is to find a new host. So they just keep mutating, and some of them dont work. Most of them fortunately dont work, but a lot of them do, and those are what were seeing.

Meanwhile, globally, were still giving COVID as many opportunities to evolve as we were a year ago if not more because now there are reinfections.Yeah, if not more. Were putting pressure on the virus to find new ways to circumvent our immune response and thats what it continues to do.

And at the same time, weve collectively done virtually nothing to prepare for whatever evolves next.Right. From day one of this pandemic, we have never tried to get ahead of the virus. Labs have come up with all sorts of broad neutralizing antibodies that would be variantproof. Nasal vaccines, to block transmission, to achieve mucosal immunity there are 12 in clinical trials. There are all these drugs in the hopper. Pan-coronavirus vaccines. These are all academic pursuits or largely from small companies. There hasnt been a national or a much larger international initiative to get ahead of the virus.

By initiative, you mean money.Money and an Operation Warp Speed 2, with collaborations and private-public industry partnerships. And not necessarily just the U.S., it should be global. But you dont see that, and its so stupid because look how successful we were. Operation Warp Speed showed how good we could be at this. But we havent done anything. We keep reacting and chasing instead of doing the things we know would get ahead of it.

I look at the data, and it says we can do better than this. I know we can; the science is there. Its just waiting in the hopper to be activated, but were just not taking it seriously enough. And I want to get out of this thing. I thought we were out of it as we came down with Delta in June 2021. Who wouldve thought we would get to now, a year-plus later, and theres still no light ahead of us? Thats why I want to take the aggressive get-ahead stance.

It seems like political will for that stance is nonexistent in the U.S. right now.Its also internationally. You dont see the U.K. which has been a model for science in the pandemic or many places around the world that are capable of it talking about going after pan-coronavirus vaccines. Why arent we making this a global priority?

Im optimistic that we can seize and achieve containment of the virus once and for all. Ive been optimistic like that for many months, but I feel like Im a Lone Ranger not a single voice, but one of a minority.

To be clear, you mean a pharmacological way to contain the virus. Because were never going back to nonpharmaceutical interventions like we saw in the first few years of the pandemic, or at least unless theres an enormous rise in hospitalizations and deaths.Yeah. In January 2021, my colleague Dennis Burton and I wrote in Nature that we need a variantproof vaccine. This virus is ideally suited, as compared to flu or HIV, for a variantproof vaccine. The initial success of Pfizers vaccine was 95 percent against symptomatic COVID. Theres never been a flu vaccine like that. Look at the success of Paxlovid: a 90 percent reduction in hospitalizations and deaths. This virus is vulnerable. Weve proven that. Were just not building on our successes. Its incredible. This is a less challenging, less hypermutating virus than the flu. Our COVID vaccines make flu vaccines look like a joke, or at least they did.

So we already have COVID on the ropes and can finish it off if we try.Thats why Im so optimistic. We can do this. But were not doing it.

This interview has been edited for length and clarity.

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BA.5 Shows COVID Is Evolving Fast. Why Aren't We Fighting Back? - New York Magazine

Last Christmas, as the Omicron variant was ricocheting around the United States, Mary Carrington unknowingly found herself at a superspreader eventan indoor party, packed with more than 20 people, at least one of whom ended up transmitting the virus to most of the gatherings guests.

After two years of avoiding the coronavirus, Carrington felt sure that her time had come: Shed been holding her great-niece, who tested positive soon after, and she was giving me kisses, Carrington told me. But she never caught the bug. And I just thought, Wow, I might really be resistant here. She wasnt thinking about immunity, which she had thanks to multiple doses of a COVID vaccine. Rather, perhaps via some inborn genetic quirk, her cells had found a way to naturally repel the pathogens assaults instead.

Carrington, of all people, understood what that would mean. An expert in immunogenetics at the National Cancer Institute, she was one of several scientists who, beginning in the 1990s, helped uncover a mutation that makes it impossible for most strains of HIV to enter human cells, rendering certain people essentially impervious to the pathogens effects. Maybe something analogous could be safeguarding some rare individuals from SARS-CoV-2 as well.

Read: America is running out of COVID virgins

The idea of coronaviral resistance is beguiling enough that scientists around the world are now scouring peoples genomes for any hint that it exists. If it does, they could use that knowledge to understand whom the virus most affects, or leverage it to develop better COVID-taming drugs. For individuals who have yet to catch the contagiona fast-dwindling proportion of the populationresistance dangles like a superpower that people cant help but think they must have, says Paula Cannon, a geneticist and virologist at the University of Southern California.

As with any superpower, though, bona fide resistance to SARS-CoV-2 infection would likely be very rare, says Helen Su, an immunologist at the National Institutes of Allergy and Infectious Disease. Carringtons original hunch, for one, eventually proved wrong: She recently returned from a trip to Switzerland and found herself entwined with the virus at last. Like most people who remained unscathed until recently, Carrington had done so for two and a half years through a probable combination of vaccination, cautious behavior, socioeconomic privilege, and luck. Its entirely possible that inborn coronavirus resistance may not even existor that it may come with such enormous costs that its not worth the protection it theoretically affords.

Of the 1,400 or so viruses, bacteria, parasites, and fungi known to cause disease in humans, Jean-Laurent Casanova, a geneticist and an immunologist at Rockefeller University, is certain of only three that can be shut out by bodies with one-off genetic tweaks: HIV, norovirus, and a malaria parasite.

The HIV-blocking mutation is maybe the most famous. About three decades ago, researchers, Carrington among them, began looking into a small number of people who we felt almost certainly had been exposed to the virus multiple times, and almost certainly should have been infected, and yet had not, she told me. Their superpower was simple: They lacked functional copies of a gene called CCR5, which builds a cell-surface protein that HIV needs in order to hack its way into T cells, the viruss preferred human prey. Just 1 percent of people of European descent harbor this mutation, called CCR5-32, in two copies; in other populations, the trait is rarer still. Even so, researchers have leveraged its discovery to cook up a powerful class of antiretroviral drugs, and purged the virus from two people with the help of 32-based bone-marrow transplantsthe closest that medicine has come to developing a functional HIV cure.

The stories with those two other pathogens are similar. Genetic errors in a gene called FUT2, which pastes sugars onto the outsides of gut cells, can render people resistant to norovirus; a genomic tweak erases a protein called Duffy from the walls of red blood cells, stopping Plasmodium vivax, one of several parasites that causes malaria, from wresting its way inside. The Duffy mutation, which affects a gene called DARC/ACKR1, is so common in parts of sub-Saharan Africa that those regions have driven rates of P. vivax infection way down.

In recent years, as genetic technologies have advanced, researchers have begun to investigate a handful of other infection-resistance mutations against other pathogens, among them hepatitis B virus and rotavirus. But the links are tough to definitively nail down, thanks to the number of people these sorts of studies must enroll, and to the thorniness of defining and detecting infection at all; the case with SARS-CoV-2 will likely be the same. For months, Casanova and a global team of collaborators have been in contact with thousands of people from around the world who believe they harbor resistance to the coronavirus in their genes. The best candidates have had intense exposures to the virussay, via a symptomatic person in their homeand continuously tested negative for both the pathogen and immune responses to it. But respiratory transmission is often muddied by pure chance; the coronavirus can infiltrate people silently, and doesnt always leave antibodies behind. (The team will be testing for less fickle T-cell responses as well.) People without clear-cut symptoms may not test at all, or may not test properly. And all on its own, the immune system can guard people against infection, especially in the period shortly after vaccination or illness. With HIV, a virus that causes chronic infections, lacks a vaccine, and spreads through clear-cut routes in concentrated social networks, it was easier to identify those individuals whom the virus had visited but not put down permanent roots within, says Ravindra Gupta, a virologist at the University of Cambridge. SARS-CoV-2 wont afford science the same ease of study.

Read: Is BA.5 the reinfection wave?

A full analogue to the HIV, malaria, and norovirus stories may not be possible. Genuine resistance can manifest in only so many ways, and tends to be born out of mutations that block a pathogens ability to force its way into a cell, or xerox itself once its inside. CCR5, Duffy, and the sugars dropped by FUT2, for instance, all act as microbial landing pads; mutations rob the bugs of those perches. If an equivalent mutation exists to counteract SARS-CoV-2, it might logically be found in, say, ACE2, the receptor that the coronavirus needs in order to break into cells, or TMPRSS2, a scissors-like protein that, for at least some variants, speeds the invasive process along. Already, researchers have found that certain genetic variations can dial down ACE2s presence on cells, or pump out junkier versions of TMPRSS2hints that there could be tweaks that further strip away the molecules. But ACE2 is very important to blood-pressure regulation and the maintenance of lung-tissue health, said Su, of NIAID, whos one of many scientists collaborating with Casanova to find SARS-CoV-2 resistance genes. A mutation that keeps the coronavirus out might very well muck around with other aspects of a persons physiology. That could make the genetic tweak vanishingly rare, debilitating, or even, as Gupta put it, not compatible with life. People with the CCR5-32 mutation, which halts HIV, are basically completely normal, Cannon told me, which means HIV kind of messed up in choosing CCR5. The coronavirus, by contrast, has figured out how to exploit something vital to its hostan ingenious invasive move.

The superpowers of genetic resistance can have other forms of kryptonite. A few strains of HIV have figured out a way to skirt around CCR5, and glom on to another molecule, called CXCR4; against this version of the virus, even people with the 32 mutation are not safe. A similar situation has arisen with Plasmodium vivax, which we do see in some Duffy-negative individuals, suggesting that the parasite has found a back door, says Dyann Wirth, a malaria researcher at Harvards School of Public Health. Evolution is a powerful strategyand with SARS-CoV-2 spewing out variants at such a blistering clip, I wouldnt necessarily expect resistance to be a checkmate move, Cannon told me. BA.1, for instance, conjured mutations that made it less dependent on TMPRSS2 than Delta was.

Read: The BA.5 wave is what COVID normal looks like

Still, protection doesnt have to be all or nothing to be a perk. Partial genetic resistance, too, can reshape someones course of disease. With HIV, researchers have pinpointed changes in groups of so-called HLA genes that, through their impact on assassin-like T cells, can ratchet down peoples risk of progressing to AIDS. And a whole menagerie of mutations that affect red-blood-cell function can mostly keep malaria-causing parasites at baythough many of these changes come with a huge human cost, Wirth told me, saddling people with serious clotting disorders that can sometimes turn lethal themselves.

With COVID-19, too, researchers have started to home in on some trends. Casanova, at Rockefeller, is one of several scientists who has led efforts unveiling the importance of an alarm-like immune molecule called interferon in early control of infection. People who rapidly pump out gobs of the protein in the hours after infection often fare just fine against the virus. But those whose interferon responses are weak or laggy are more prone to getting seriously sick; the same goes for people whose bodies manufacture maladaptive antibodies that attack interferon as it passes messages between cells. Other factors could toggle the risk of severe disease up or down as well: cells ability to sense the virus early on; the amount of coordination between different branches of defense; the brakes the immune system puts on itself, so it does not put the hosts own tissues at risk. Casanova and his colleagues are also on the hunt for mutations that might alter peoples risk of developing long COVID and other coronaviral consequences. None of these searches will be easy. But they should be at least simpler than the one for resistance to infection, Casanova told me, because the outcomes theyre measuringserious and chronic forms of diseaseare that much more straightforward to detect.

If resistance doesnt pan out, that doesnt have to be a letdown. People dont need total blockades to triumph over microbesjust a defense thats good enough. And the protection were born with isnt all the leverage weve got. Unlike genetics, immunity can be easily built, modified, and strengthened over time, particularly with the aid of vaccines. Those DIY defenses are probably what kept Carringtons case of COVID down to a mild course, she told me. Immune protection is also a far surer bet than putting a wager on what we may or may not inherit at birth. Better to count on the protections we know we can cook up ourselves, now that the coronavirus is clearly with us for good.

Read this article:

Could Genetics Be the Key to Never Getting the Coronavirus? - The Atlantic

Good evening. Im Karen Kaplan, and its Tuesday, July 26. Heres the latest on whats happening with the coronavirus in California and beyond.

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Were still in a pandemic. The number of coronavirus infections is high and rising. But something fundamental about COVID-19 has changed: It isnt as scary anymore.

Over the last week, the U.S. has averaged a whopping 120,000 new cases per day. (And those are just the ones reported to authorities; the true number is even higher.)

Contrast that to the early weeks of the outbreak, when society all but shut down in an effort to steer clear of the virus and bend the curve. All it took to get our attention back then was fewer than 30,000 cases per day.

They say familiarity breeds contempt, but in this case its having the opposite effect. The more time we spend with the coronavirus, the less we seem to worry about it.

Indeed, infections are now so commonplace that the fear of the unknown is fading, said Dr. Peter Chin-Hong, an infectious diseases expert at UC San Francisco.

You get it yourself and know tons of people who got it, and you fear it less, he said.

That explains why face masks were few and far between among the shoppers packed into the air-conditioned Westfield Valencia Town Center in Santa Clarita on a recent hot summer day, my colleagues Rebecca Schneid, Heidi Prez-Moreno and Hailey Brandon-Potts report.

People are just exasperated and over it, said Hailey Jimenez, 21, who was mask-free during a recent shift tending a jewelry kiosk there. I know Im over it.

Nicki Spravka knows the feeling. The 20-year-old moved from store to store without a mask or much angst.

I go to school in Colorado, and basically for the past year people have been acting like it doesnt exist anymore, she said of the virus. I mean, I guess I care. But it feels like what we do isnt really going to affect it because infections are still going to happen.

People, with and without masks, shop in L.A.'s Santee Alley in mid-July.

(Irfan Khan / Los Angeles Times)

This attitude is not unique to California or the West. The Pew Research Centers most recent survey about Americans attitudes about the pandemic found that only 41% considered the coronavirus a major threat to public health. Thats the lowest figure Pew has ever recorded. (An additional 45% considered the virus a minor threat and 13% called it not a threat.)

Likewise, only 34% of respondents were either somewhat or very concerned that the virus would land them in the hospital, and 50% were somewhat or very concerned that theyd spread an infection to someone else. Those figures also represent all-time lows for the pandemic.

Nationwide, daily COVID-19 deaths have averaged around 365 over the last week. The count hasnt been that low for a year, since the lull before the Delta surge. The only other time it has been lower was the initial weeks of the outbreak. So perhaps there is less reason to fear the coronavirus.

If your metric is infections, it looks hopeless, Chin-Hong said. But if your metric is people getting seriously ill and dying wow, thats a huge victory.

For the most part, the public is focused on the latter metric. But the health establishment is mostly focused on the former, especially the speed with which new variants are emerging and the possibility that one of them will be impervious to our vaccines and treatments, effectively sending us back to square one.

That helps explain why Los Angeles County is probably on the verge of reinstating an indoor mask mandate. Unless conditions substantially improve in the next couple of days, the county is likely to learn Thursday that it is entering its third consecutive week with a high COVID-19 community level because it has more 200 new infections and more than 10 new COVID-19 hospital admissions per 100,000 people over the last seven days. (As of last Thursday, there were 481 new infections and 11.4 new hospital admissions per 100,000 people per week.)

Bringing those numbers down is necessary to protect the vulnerable among us, such as the elderly and people who are immunocompromised, said Dr. Robert Kim-Farley, an epidemiologist and infectious diseases expert at UCLA.

What we need to do is have a mindset, or social norm, that we are going to expect somewhat of a roller-coaster ride as new variants arise and sweep through the population, he said. We can go back to more business as usual, but when rates are high, we should all do our part in reducing transmission.

Julisa Carrillo hopes people hear that message. She was hospitalized because of COVID-19 twice before the vaccines became available. Both of those hospitalizations included time on a ventilator.

More than a year and a half later, her lungs still dont feel the same. In her view, wearing a mask feels like a reasonable trade-off to help people avoid that same fate.

This is a virus that is hurting so many people, she said as she waited for a bus in Huntington Park. I myself dont feel safe.

California cases and deaths as of 6:30 p.m. Tuesday:

Track Californias coronavirus spread and vaccination efforts including the latest numbers and how they break down with our graphics.

The coronavirus can come for anyone, even the leader of the free world. Then-President Trumps illness in 2020 may have seemed like a bit of bad luck though if were being honest, his White House wasnt being particularly careful but current President Bidens diagnosis confirms that even those who take abundant precautions are vulnerable.

But its not all bad news for Biden. Catching the coronavirus in the summer of 2022 is not at all like catching it in the fall of 2020, my colleague Melissa Healy reports. Unlike Trump, Biden is benefiting from a full 2 years of scientific and medical advances against the once-novel virus. Plus, the virus itself has changed in ways that make it harder to evade but easier to survive.

Biden said Monday that hes feeling better every day. His schedule is lighter than it would have been while hes isolating at the White House, but Im meeting all my requirements that have come before me, he said.

Heres a look at the many advantages for Biden and the roughly 850,000 other Americans who caught the virus in the last week that werent available to Trump:

VACCINES: When Trump was diagnosed in early October 2020, the first COVID-19 vaccine from Pfizer and BioNTech was more than two months away from being authorized for emergency use by the Food and Drug Administration.

By the time Biden was diagnosed, he had received two primary doses of the companies Comirnaty vaccine, plus two booster doses. His most recent shot was on March 30. A letter from Dr. Kevin C. OConnor, the White House physician, described him as maximally protected.

Im doing well, getting a lot of work done, he said in a video. (Hes following Dr. Anthony Faucis lead and trying to power through instead of taking the time to rest and recover.)

Biden himself credited his four shots for his mild illness. His symptoms included a runny nose, cough, sore throat and some body aches.

Data from the Centers for Disease Control and Prevention back him up. Among Americans 65 and older, those who are unvaccinated are 3.8 times more likely to wind up hospitalized with COVID-19 than those who have been vaccinated and boosted at least once.

Whats more, people in Bidens age group 65 to 79 who are unvaccinated are nearly 9 times more likely to die of COVID-19 than their counterparts who are vaccinated and boosted. The second booster is important: The risk of death for Americans 50 and older who received it was four times lower than for their peers who stopped at one booster.

President Biden receives his first booster dose of Pfizer and BioNTechs COVID-19 vaccine on Sept. 27, 2021.

(Anna Moneymaker / Getty Images)

TREATMENTS: By the time Bidens illness was announced, he had already begun a course of Paxlovid. In clinical trials, patients at high risk of becoming severely ill were 88% less likely to be hospitalized or die if they took the antiviral (which is administered in pill form over five days). Biden falls into the high risk category because of his age (hell turn 80 in November).

Paxlovid received emergency use authorization in December, more than a year after Trumps bout with COVID-19. After initial shortages, it is now available at test to treat sites around the country, and as of this month, pharmacists have clearance to prescribe it to patients.

Should Biden take a turn for the worse and develop symptoms such as low oxygen levels, blood clots or problems with his heart or kidney function, there are plenty of other tools available to his doctors.

Remdesivir, which was given to Trump, would be available as a backstop, said Dr. Roy M. Gulick, who co-chaired the National Institutes of Healths panel on COVID-19 treatment guidelines. Today, physicians could also turn to one or more of the specialized drugs that calm an overactive immune system; although these were developed to treat other diseases, theyve been found to help those with COVID-19 as well.

Doctors have refined a variety of treatments while tending to Americas 90-million-plus patients over the course of the pandemic, Gulick said. For instance, theyre quicker to prescribe blood thinners for hospitalized patients to reduce the risk of blood clots. Theyve streamlined their use of steroids. Theyre more cautious about putting patients with breathing difficulties on ventilators, since they have the potential to do more harm than good. Theyve also figured out how to position patients with obesity to help keep their airways clear.

So much has changed since Trump got COVID, Gulick said. We have made substantive progress in treating people with severe COVID who are admitted to hospital, and fewer are dying as a result.

THE VIRUS ITSELF: We may lament the seemingly endless parade of variants and subvariants. But if you had to be infected with the SARS-CoV-2 coronavirus, youd rather have a version of Omicron than the original strain from Wuhan, China.

Trump fell ill before the emergence of the Alpha variant in the U.K., so its a safe bet that he was sickened by a virus that closely resembled the one that left China in late 2019. Virtually all of the SARS-CoV-2 coronaviruses circulating in the U.S. today are some version of Omicron, with the BA.5 subvariant alone accounting for an estimated 82% of specimens, according the CDC, and OConnor said thats probably the strain that got Biden.

For most of the pandemic, the COVID-19 death rate among those infected stood at about 2% of reported cases. But that figure dropped significantly after Omicron arrived, according to Beth Blauer, an associate vice provost at Johns Hopkins University. Now, fewer than 0.5% of reported infections results in death.

Population immunity from vaccines and past infections may help explain that progress, she wrote, but the data trends clearly demonstrate that Omicron is a much less deadly variant.

See the latest on Californias vaccination progress with our tracker.

Through parts of June, Los Angeles County and the San Francisco Bay Area had similar COVID-19 mortality rates. Then July came along, and deaths rose in L.A. but that increase was not matched up north.

As of Monday, the Bay Area had 56 deaths per 10 million residents over the last week. L.A. County, meanwhile, recorded 96 deaths per 10 million residents in the same period, a figure that was 70% higher.

Its not clear why deaths went up here but not there. L.A. has a higher poverty rate and more overcrowded housing. That means if one member of a household is infected, the number of people at risk of exposure is greater. Vaccination rates are also lower here than they are up north. According to The Times tracker, 73.7% of L.A. County residents are fully vaccinated; that percentage is lower than in all but one Bay Area county (Solano).

There are hints that L.A.'s death toll may begin to fall soon. The official count of new infections here has begun to decline, as has the number of infected patients in the countys hospitals. Last Wednesday, that number stood at 1,329; by Friday, it was down to 1,200, before rising somewhat to 1,286 on Monday.

As for coronavirus cases, the county was averaging about 6,100 infections per day over the week that ended Monday. During the previous week, the average number of daily infections was nearly 6,900.

Those improved trend lines are fueling hope that L.A. County Public Health Director Barbara Ferrer might not implement an indoor mask mandate later this week even if the county still has a high COVID-19 community level.

Should we see sustained decreases in cases, or the rate of hospital admissions moves closer to the threshold for medium, we will pause implementation of universal indoor masking as we closely monitor our transmission rates, Ferrer said. No decision will be made until after the CDC updates its community-level assessments on Thursday.

Officials in Beverly Hills would be happy to see the county demur on a mask mandate. The City Council voted unanimously Monday night not to enforce an indoor mask rule, should one materialize.

I support the power of choice, Mayor Lili Bosse said in a statement. This is a united City Council and community that cares about health. We are not where we were in 2020, and now we need to move forward as a community and be part of the solution.

Restaurants and bars, on the other hand, are already bracing for the stink eye they expect to get from customers if they have to go back to enforcing an indoor mask mandate. The job will be even more difficult this time around because the BA.5 subvariant has forced eating and drinking establishments to operate with skeletal staffing.

Im fearful and Im nervous and theres a lot of anxiety behind it, said Robert Fleming, who opened the Capri Club bar in Eagle Rock in June.

Plenty of other employers are dealing with COVID-induced staffing shortages too. Notable among them is the Transportation Security Administration.

The L.A. County health department says at least 233 cases have been confirmed among TSA workers at Los Angeles International Airport since June 9. The federal agency acknowledged an outbreak at LAX but said the figures released by the county overstated the current state of infections.

President Biden wasnt the only politico to catch the coronavirus in the last week. Democratic Sen. Joe Manchin III of West Virginia tweeted Monday that he tested positive for an infection and was experiencing mild COVID-19 symptoms. His Republican colleague Sen. Lisa Murkowski of Alaska tweeted similar news Monday and said she was experiencing flu symptoms.

On the research front, a study from USC has identified some new potential risk factors for developing long COVID. Like previous studies, the analysis found that patients who had obesity prior to their illnesses were more likely to have the lingering symptoms associated with long COVID. The USC team also found that patients who had sore throats, headaches and hair loss after becoming infected with the coronavirus were more likely to have long COVID.

The researchers dont think hair loss itself causes long COVID. Rather, they suspect that hair loss reflects extreme stress, potentially a reaction to a high fever or medications, said Eileen Crimmins, a demographer at USCs Leonard Davis School of Gerontology who worked on the study that appeared in Scientific Reports. So its probably some indication of how severe the illness was.

Separately, a pair of studies by an international team of experts used different analytical approaches to home in on the epicenter of the pandemic that has killed more than 6.4 million people around the world. Both methods point to the same conclusion: The coronavirus probably jumped from animals to humans at the Huanan Wholesale Seafood Market in Wuhan, China. In fact, it probably happened at least twice.

Several researchers who worked on the new papers had been open to the possibility that the virus had escaped from a Wuhan lab. But sleuthing over the last year or so has convinced them that the market is a far more plausible culprit.

In a city covering more than 3,000 square miles, the area with the highest probability of containing the home of someone who had one of the earliest COVID-19 cases in the world was an area of a few city blocks, with the Huanan market smack dab inside it, said one of those researchers, University of Arizona virologist Michael Worobey.

And finally, it looks as though there are no countries left that have more than 100,000 people but are still coronavirus-free. The island nation of Micronesia (population 115,000) appears to have been the last to fall and its outbreak is a doozy. It began last week and has already spread to at least 1,261 people. Eight people have been hospitalized with COVID-19, and one has died.

Turkmenistan is now the only remaining country with a population of at least 100,000 and no official coronavirus cases. Outside experts believe, however, that the virus is there and the countrys autocratic leaders are simply ignoring it.

Todays question comes from readers who want to know: Should I let the county health department know that I got a positive result on a rapid test?

If you live in L.A. County, you dont have to.

That said, there are some calls you should make. If you have a regular healthcare provider, let them know that youve tested positive.

You should also inform your recent close contacts so they can be tested. A close contact is someone whos been within 6 feet of you for a total of 15 minutes over a 24-hour period. Anyone who fits that bill in the two days leading up to your first COVID-19 symptoms or your positive test result (whichever came first) deserves to hear from you.

If you need help tracking down your close contacts, you actually do have a good reason to call the L.A. County Department of Public Health. The department has set up a hotline to assist residents with issues like these. The folks there can also answer questions you may have and can help you get a prescription for an antiviral medication, if warranted. The number for the hotline is (833) 540-0473.

The county health department is keeping track of the positive home test results they hear about. But a spokeswoman told my colleagues Jon Healey and Karen Garcia that department officials dont need you to tell them that youve tested positive and they definitely dont want you to tell them if youve tested negative.

Its not just that health officials are too busy to take your call. Its that they cant gauge the reliability of the home test you (and everyone else) used, or whether you (and everyone else) used it correctly. Thats why they tally only the results of tests performed in a laboratory.

L.A. County is hardly alone in this regard even the CDC takes this approach.

We want to hear from you. Email us your coronavirus questions, and well do our best to answer them. Wondering if your questions already been answered? Check out our archive here.

(Mariah Tauger / Los Angeles Times)

The hands in the photo above belong to chef Genet Agonafer. Shes the proprietor of Meals by Genet, the bistro in L.A.'s Little Ethiopia that helped make the berbere-centered flavors of her native country one of the important pieces of the mosaic that defines Los Angeles cuisine, as my colleague Laurie Ochoa writes.

Ochoa selected Agonafer as The Times 2022 Gold Award honoree. The award is bestowed not just for excellent cooking but also for broadening our culinary horizons.

In light of this praise, you might expect Meals by Genet to have a packed dining room. But when restaurants were able to reopen their dining rooms, Agonafer decided to keep hers closed. (She makes occasional exceptions for weddings and other private parties.) She hadnt missed the stress of full-on restaurant work, but she didnt want to close down altogether. So she opted for a compromise, offering takeout dinners on Thursdays through Sundays.

Although the limited hours mean less money, Agonafer said its a worthy trade-off.

Everything is just peaceful and easygoing, she said. There is still that stress when the rush happens or when we have events here, but things are going so incredibly well.

Resources

Need a vaccine? Heres where to go: City of Los Angeles | Los Angeles County | Kern County | Orange County | Riverside County | San Bernardino County | San Diego County | San Luis Obispo County | Santa Barbara County | Ventura County

Practice social distancing using these tips, and wear a mask or two.

Watch for symptoms such as fever, cough, shortness of breath, chills, shaking with chills, muscle pain, headache, sore throat and loss of taste or smell. Heres what to look for and when.

Need to get a test? Testing in California is free, and you can find a site online or call (833) 422-4255.

Americans are hurting in various ways. We have advice for helping kids cope, as well as resources for people experiencing domestic abuse.

Weve answered hundreds of readers questions. Explore them in our archive here.

For our most up-to-date coverage, visit our homepage and our Health section, get our breaking news alerts, and follow us on Twitter and Instagram.

See more here:

Coronavirus Today: Out of patience with pandemic precautions - Los Angeles Times

The House passed a bill on Tuesday to allow a government agency to award grants into the cognitive effects of COVID-19.

The legislation, titled the Brycen Gray and Ben Price COVID-19 Cognitive Research Act, passed in a 350-69 vote, with all opposition coming from Republicans. Eight Republicans and four Democrats did not vote.

The measure calls on the director of the National Science Foundation to award grants to eligible entities including higher education institutions or other groups made up of universities and nonprofit organizations to assist them in researching the disruption of regular cognitive processes associated with both short-term and long-term COVID-19 infections.

Research eligible under the bill includes studies on the effects COVID-19 infections have on cog4 nition, emotion, and neural structure and function as well as the influence coronavirus-related psychological and psychosocial factors have on the disruption of cognitive processes.

The grants should be awarded on a competitive, merit-reviewed basis, according to the bill.

In a statement announcing the bill in October, Rep. Anthony Gonzalez (R-Ohio), a co-sponsor of the measure, cited research from The Lancet Psychiatry that says roughly 1 in 3 patients diagnosed with COVID-19 received a neurological or psychiatric diagnosis in the six months after their positive test.

The legislation is named after Brycen Gray, 17, and Ben Price, 48, both of whom died by suicide after experiencing mental health issues following their bouts with COVID-19.

During debate on the House floor Tuesday, Gonzalez spoke about Gray and Price, saying the two tragically passed after battles with cognitive impairments caused by COVID-19.

Despite having no history of mental illness, each of them began to battle symptoms such as anxiety, panic and paranoia. The disease took Brycen and Ben from two of the healthiest, most vibrant people you could find to individuals so debilitated that they could not bear to live another day. While they fought to the bitter end, each chose to end their pain, he added.

The Ohio Republican said the bill would help learn why COVID-19 has an impact on the brain.

If we believe in protecting our families, we need to act now and start finding answers to why COVID-19 can have such a significant impact on the brain. The legislation before us today is another important step in that effort, he said.

Rep. Don Beyer (D-Va.) said researchers are raising alarms about the risk of mental health issues and suicide following COVID-19 diagnoses, adding that improved data collection and additional research is needed to better understand the mental health implications of COVID-19 infection.

Republican no votes included Reps. Rick Allen (Ga.), Jodey Arrington (Texas), Jim Banks (Ind.), Jack Bergman (Mich.), Andy Biggs (Ariz.), Dan Bishop (N.C.), Lauren Boebert (Colo.), Mo Brooks (Ala.), Ken Buck (Colo.), Tim Burchett (Tenn.), Michael Burgess (Texas), Kat Cammack (Fla.), Madison Cawthorn (N.C.), Ben Cline (Va.), Michael Cloud (Texas), Andrew Clyde (Ga.), James Comer (Ky.), Warren Davidson (Ohio), Scott DesJarlais (Tenn.), Byron Donalds (Fla.), Ron Estes (Kan.), Pat Fallon (Texas), Scott Fitzgerald (Wisc.), Virginia Foxx (N.C.), Russ Fulcher (Idaho), Matt Gaetz (Fla.), Louie Gohmert (Texas), Bob Good (Va.), Lance Gooden (Texas), Paul Gosar (Ariz.), Mark Green (Tenn.), Marjorie Taylor Greene (Ga.), Morgan Griffith (Va.), Glenn Grothman (Wisc.), Andy Harris (Md.), Diana Harshbarger (Tenn.), Kevin Hern (Okla.), Yvette Herrell (N.M.), Jody Hice (Ga.), Clay Higgins (La.), Ashley Hinson (Iowa), Darrell Issa (Calif.), Ronny Jackson (Texas), Mike Johnson (La.), Jim Jordan (Ohio), John Joyce (Pa.), Debbie Lesko (Ariz.), Barry Loudermilk (Ga.), Nicole Malliotakis (N.Y.), Tracey Mann (Kan.), Thomas Massie (Ky.), Brian Mast (Fla.), Tom McClintock (Calif.), Dan Meuser (Pa.), Marry Miller (Ill.), Barry Moore (Ala.), Troy Nehls (Texas), Ralph Norman (S.C.), Greg Pence (Ind.), Scott Perry (Pa.), August Pfluger (Texas), Chip Roy (Texas), David Schweikert (Ariz.), Mike Simpson (Idaho), Van Taylor (Texas), Claudia Tenney (N.Y.), Tom Tiffany (Wisc.), Jeff Van Drew (N.J.) and Beth Van Duyne (Texas).

Link:

House passes bill for research on cognitive effects of coronavirus, 69 Republicans vote no - The Hill

The world has experienced a slew of surges caused by an alphabet of variants since the onset of the COVID-19 pandemic in March 2020. Thankfully, none of the variants has led to a significant increase in disease severity.

Becker's spoke to Jonathan Abraham, MD, PhD, an infectious diseases physician at Boston-based Brigham & Women's Hospital, to learn more about why the SARS-CoV-2 virus's evolution hasn't led to significant changes in disease severity from the ancestral strain, and what are the chances that it eventually mutates to cause severe illness.

"It's something that even as a scientific community, we don't understand yet," Dr. Abraham said. He is an assistant professor of microbiology at Harvard Medical School and runs the Abraham Lab, which studies how pathogens interact with the cells of their hosts.

Two questions that remain:

When will immunity significantly wane?

While each new variant appears to be better at infecting vaccinated people than the last, vaccines have still largely protected against severe illness from each of them.

The question of whether the SARS-CoV-2 virus could eventually evolve to cause more severe illness then depends, at least in part, on the level of immunity a population has.

"Overtime, we've seen this virus mutate and mutate, but the question is still when will the immunity we have either from vaccines or from prior exposure [wane,] and by then, will the virus have disappeared or will it have continued to mutate?" said Dr. Abraham.

If the virus continues to mutate over time and the population's immunity wanes significantly, more severe disease is a possibility, "but the question is really hard to separate from one of the infected host, which has some degree of immunity," he said.

In a vaccine-less world where there were no levels of immunity and a mutating virus, variants like omicron would likely cause severe illness. But in a world where most people have been vaccinated or previously infected, that's not the case.

Could the virus evolve to evade T-cell responses?

Even with the virus able to evade antibodies, there is evidence that T-cells a separate arm of the immune system's response play a role in maintaining immunity from COVID-19.

In someone with prior immunity from vaccination, infection or both, "I think most would believe T-cells probably account for why disease severity is not as significant when someone gets infected now," Dr. Abraham said.

"T-cells are really the work horses that may be protecting us from getting sicker," he said, but if the virus mutates in a way that allows it to evade both antibody and T-cell responses, that may be a recipe for more severe disease.

Some research has shown people who have COVID-19 generate T-cells that target at least 15 to 20 different fragments of SARS-CoV-2 virus' protein, according to a Nature report. The targeted protein fragments can vary widely among different people, meaning a population could generate a broad variety of T-cells against the virus.

"That makes it very hard for the virus to escape cell recognition," Dr. Alessandro Sette at the La Jolla Institute for Immunology in California, told the news outlet, adding its "unlike the situation for antibodies."

Read the rest here:

2 questions a Harvard infectious disease expert still has about the coronavirus' evolution - Becker's Hospital Review

NEW YORK and MAINZ, Germany, July 27, 2022 Pfizer Inc. (NYSE: PFE) and BioNTech SE (Nasdaq: BNTX) today announced that the companies have initiated a randomized, active-controlled, observer-blind, Phase 2 study to evaluate the safety, tolerability, and immune response of an enhanced COVID-19 mRNA-based vaccine candidate at a 30 g dose level. This next-generation bivalent COVID-19 vaccine candidate, BNT162b5, consists of RNAs encoding enhanced prefusion spike proteins for the SARS-CoV-2 ancestral strain (wild-type) and an Omicron variant. The enhanced spike protein encoded from the mRNAs in BNT162b5 has been modified with the aim of increasing the magnitude and breadth of the immune response that could better protect against COVID-19.

This is the first of multiple vaccine candidates with an enhanced design which the companies plan to evaluate as part of a long-term scientific COVID-19 vaccine strategy to potentially generate more robust, longer-lasting, and broader immune responses against SARS-CoV-2 infections and associated COVID-19.

BNT162b5 will be evaluated in a U.S.-based study enrolling approximately 200 participants aged between 18 and 55 who have received one booster dose of a U.S.-authorized COVID-19 vaccine at least 90 days prior to their first study visit. Participants will be stratified by the number of months since their last dose of COVID-19 vaccine received prior to entering the study (three to six months or more than six months). The study does not include a placebo (injection with no active ingredient). For more information about this study please visit http://www.clinicaltrials.govon this link.

The Pfizer-BioNTech COVID-19 Vaccine, BNT162b2, which is based on BioNTechs proprietary mRNA technology, was developed by both BioNTech and Pfizer. BioNTech is the Marketing Authorization Holder in the United States, the European Union, the United Kingdom, Canada and other countries, and the holder of emergency use authorizations or equivalents in the United States (jointly with Pfizer) and other countries. Submissions to pursue regulatory approvals in those countries where emergency use authorizations or equivalent were initially granted are planned.

U.S. Indication & Authorized Use

Pfizer-BioNTech COVID-19 Vaccine is FDA authorized under Emergency Use Authorization (EUA) for active immunization to prevent coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in individuals 6 months of age and older.

Pfizer-BioNTech COVID-19 Vaccine is FDA authorized to provide:

Primary Series

Booster Series

COMIRNATY INDICATIONCOMIRNATY (COVID-19 Vaccine, mRNA) is a vaccine approved for active immunization to prevent coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in individuals 12 years of age and older.

COMIRNATY AUTHORIZED USESCOMIRNATY (COVID-19 Vaccine, mRNA) is FDA authorized under Emergency Use Authorization (EUA) to provide:

Primary Series

Booster Dose

Emergency Use AuthorizationEmergency uses of the vaccine have not been approved or licensed by FDA, but have been authorized by FDA, under an Emergency Use Authorization (EUA) to prevent Coronavirus Disease 2019 (COVID 19) in individuals 6 months of age and older. The emergency uses are only authorized for the duration of the declaration that circumstances exist justifying the authorization of emergency use of the medical product under Section 564(b)(1) of the FD&C Act unless the declaration is terminated or authorization revoked sooner.

INTERCHANGEABILITYFDA-approved COMIRNATY (COVID-19 Vaccine, mRNA) and the Pfizer-BioNTech COVID-19 Vaccine FDA authorized for Emergency Use Authorization (EUA) for individuals 12 years of age and older can be used interchangeably by a vaccination provider when prepared according to their respective instructions for use.

The formulations of the Pfizer-BioNTech COVID-19 Vaccine authorized for use in individuals 6 months through 4 years of age, 5 through 11 years of age, and 12 years of age and older are different and should therefore not be used interchangeably. The Pfizer-BioNTech COVID-19 Vaccine authorized for use in children 6 months through 11 years of age should not be used interchangeably with COMIRNATY (COVID-19 Vaccine, mRNA).

IMPORTANT SAFETY INFORMATION

Tell your vaccination provider about all of the vaccine recipients medical conditions, including if the vaccine recipient:

Pfizer-BioNTech COVID-19 Vaccine or COMIRNATY (COVID-19 Vaccine, mRNA) may not protect all vaccine recipients

Seek medical attention right away if the vaccine recipient has any of the following symptoms:

Seek medical attention right away if the vaccine recipient has any of the following symptoms after receiving the vaccine, particularly during the 2 weeks after receiving a vaccine dose:

These may not be all the possible side effects of the vaccine. Call the vaccination provider or healthcare provider about bothersome side effects or side effects that do not go away.

Click for Fact Sheets and Prescribing Information for individuals 6 months of age and older:

About Pfizer: Breakthroughs That Change Patients LivesAt Pfizer, we apply science and our global resources to bring therapies to people that extend and significantly improve their lives. We strive to set the standard for quality, safety and value in the discovery, development and manufacture of health care products, including innovative medicines and vaccines. Every day, Pfizer colleagues work across developed and emerging markets to advance wellness, prevention, treatments and cures that challenge the most feared diseases of our time. Consistent with our responsibility as one of the world's premier innovative biopharmaceutical companies, we collaborate with health care providers, governments and local communities to support and expand access to reliable, affordable health care around the world. For more than 170 years, we have worked to make a difference for all who rely on us. We routinely post information that may be important to investors on our website at http://www.Pfizer.com. In addition, to learn more, please visit us on http://www.Pfizer.com and follow us on Twitter at @Pfizer and @Pfizer News, LinkedIn, YouTube and like us on Facebook at http://www.facebook.com/Pfizer.

Pfizer Disclosure NoticeThe information contained in this release is as of July 27, 2022. Pfizer assumes no obligation to update forward-looking statements contained in this release as the result of new information or future events or developments.

This release contains forward-looking information about Pfizers efforts to combat COVID-19, the collaboration between BioNTech and Pfizer to develop a COVID-19 vaccine, the BNT162 mRNA vaccine program, and the Pfizer-BioNTech COVID-19 Vaccine, also known as COMIRNATY (COVID-19 Vaccine, mRNA) (BNT162b2) (including an enhanced mRNA-based vaccine candidate, BNT162b5, including a Phase 2 study to evaluate the safety, tolerability, and immune response of BNT162b5 at a 30-g dose level, the companies long-term scientific COVID-19 strategy, qualitative assessments of available data, potential benefits, expectations for clinical trials, potential regulatory submissions, the anticipated timing of data readouts, regulatory submissions, regulatory approvals or authorizations and anticipated manufacturing, distribution and supply) involving substantial risks and uncertainties that could cause actual results to differ materially from those expressed or implied by such statements. Risks and uncertainties include, among other things, the uncertainties inherent in research and development, including the ability to meet anticipated clinical endpoints, commencement and/or completion dates for clinical trials, regulatory submission dates, regulatory approval dates and/or launch dates, as well as risks associated with preclinical and clinical data (including Phase 1/2/3 or Phase 4 data), including any data for BNT162b2, BNT162b5, any monovalent, bivalent or variant-adapted vaccine candidates or any other vaccine candidate in the BNT162 program in any of our studies in pediatrics, adolescents, or adults or real world evidence, including the possibility of unfavorable new preclinical, clinical or safety data and further analyses of existing preclinical, clinical or safety data; the ability to produce comparable clinical or other results, including the rate of vaccine effectiveness and safety and tolerability profile observed to date, in additional analyses of the Phase 3 trial and additional studies, in real world data studies or in larger, more diverse populations following commercialization; the ability of BNT162b2, BNT162b5, any monovalent, bivalent or variant-adapted vaccine candidates or any future vaccine to prevent COVID-19 caused by emerging virus variants; the risk that more widespread use of the vaccine will lead to new information about efficacy, safety, or other developments, including the risk of additional adverse reactions, some of which may be serious; the risk that preclinical and clinical trial data are subject to differing interpretations and assessments, including during the peer review/publication process, in the scientific community generally, and by regulatory authorities; whether and when additional data from the BNT162 mRNA vaccine program will be published in scientific journal publications and, if so, when and with what modifications and interpretations; whether regulatory authorities will be satisfied with the design of and results from these and any future preclinical and clinical studies; whether and when submissions to request emergency use or conditional marketing authorizations for BNT162b5, BNT162b2 in additional populations, for a potential booster dose for BNT162b2, any monovalent, bivalent or variant-adapted vaccine candidates or any potential future vaccines (including potential future annual boosters or re-vaccination), and/or other biologics license and/or emergency use authorization applications or amendments to any such applications may be filed in particular jurisdictions for BNT162b5, BNT162b2, any monovalent or bivalent vaccine candidates or any other potential vaccines that may arise from the BNT162 program, including a potential variant-based, higher dose, or bivalent vaccine, and if obtained, whether or when such emergency use authorizations or licenses will expire or terminate; whether and when any applications that may be pending or filed for BNT162b5, BNT162b2 (including any requested amendments to the emergency use or conditional marketing authorizations), any monovalent, bivalent or variant-adapted vaccine candidates, or other vaccines that may result from the BNT162 program may be approved by particular regulatory authorities, which will depend on myriad factors, including making a determination as to whether the vaccines benefits outweigh its known risks and determination of the vaccines efficacy and, if approved, whether it will be commercially successful; decisions by regulatory authorities impacting labeling or marketing, manufacturing processes, safety and/or other matters that could affect the availability or commercial potential of a vaccine, including development of products or therapies by other companies; disruptions in the relationships between us and our collaboration partners, clinical trial sites or third-party suppliers; the risk that demand for any products may be reduced or no longer exist which may lead to reduced revenues or excess inventory; risks related to the availability of raw materials to manufacture a vaccine; challenges related to our vaccines formulation, dosing schedule and attendant storage, distribution and administration requirements, including risks related to storage and handling after delivery by Pfizer; the risk that we may not be able to successfully develop other vaccine formulations, booster doses or potential future annual boosters or re-vaccinations or new variant-based or next generation vaccines; the risk that we may not be able to maintain or scale up manufacturing capacity on a timely basis or maintain access to logistics or supply channels commensurate with global demand for our vaccine, which would negatively impact our ability to supply the estimated numbers of doses of our vaccine within the projected time periods as previously indicated; whether and when additional supply agreements will be reached; uncertainties regarding the ability to obtain recommendations from vaccine advisory or technical committees and other public health authorities and uncertainties regarding the commercial impact of any such recommendations; challenges related to public vaccine confidence or awareness; uncertainties regarding the impact of COVID-19 on Pfizers business, operations and financial results; and competitive developments.

A further description of risks and uncertainties can be found in Pfizers Annual Report on Form 10-K for the fiscal year ended December 31, 2021 and in its subsequent reports on Form 10-Q, including in the sections thereof captioned Risk Factors and Forward-Looking Information and Factors That May Affect Future Results, as well as in its subsequent reports on Form 8-K, all of which are filed with the U.S. Securities and Exchange Commission and available at http://www.sec.gov and http://www.pfizer.com.

About BioNTechBiopharmaceutical New Technologies is a next generation immunotherapy company pioneering novel therapies for cancer and other serious diseases. The Company exploits a wide array of computational discovery and therapeutic drug platforms for the rapid development of novel biopharmaceuticals. Its broad portfolio of oncology product candidates includes individualized and off-the-shelf mRNA-based therapies, innovative chimeric antigen receptor T cells, bi-specific checkpoint immuno-modulators, targeted cancer antibodies and small molecules. Based on its deep expertise in mRNA vaccine development and in-house manufacturing capabilities, BioNTech and its collaborators are developing multiple mRNA vaccine candidates for a range of infectious diseases alongside its diverse oncology pipeline. BioNTech has established a broad set of relationships with multiple global pharmaceutical collaborators, including Genmab, Sanofi, Genentech, a member of the Roche Group, Regeneron, Genevant, Fosun Pharma, and Pfizer. For more information, please visit http://www.BioNTech.com.

BioNTech Forward-looking StatementsThis press release contains forward-looking statements of BioNTech within the meaning of the Private Securities Litigation Reform Act of 1995. These forward-looking statements may include, but may not be limited to, statements concerning: BioNTechs efforts to combat COVID-19; the collaboration between BioNTech and Pfizer including the program to develop a COVID-19 vaccine and COMIRNATY (COVID-19 vaccine, mRNA) (BNT162b2) ( including a bivalent mRNA vaccine candidate, BNT162b5, including a Phase 2 study to evaluate the safety, tolerability, and immune response of BNT162b5 at the 30-g dose level, the Companies long-term scientific COVID-19 strategy, qualitative assessments of available data, potential benefits, expectations for clinical trials, the anticipated timing of regulatory submissions, regulatory approvals or authorizations and anticipated manufacturing, distribution and supply); our expectations regarding the potential characteristics of BNT162b2, BNT162b5, any monovalent or bivalent vaccine candidates or any future vaccine in our clinical trials and/or in commercial use based on data observations to date; the ability of BNT162b2, BNT162b5, any monovalent or bivalent vaccine candidates or any future vaccine, to prevent COVID-19 caused by emerging virus variants; the uncertainties inherent in research and development, including the ability to meet anticipated clinical endpoints, commencement and/or completion dates for clinical trials, regulatory submission dates, regulatory approval dates and/or launch dates, as well as risks associated with preclinical and clinical data (including Phase 1/2/3 or Phase 4 data), including the data discussed in this release for BNT162b2, BNT162b5, any monovalent or bivalent vaccine candidates or any other vaccine candidate in BNT162 program in any of our studies in pediatrics, adolescents, or adults or real world evidence, including the possibility of unfavorable new preclinical, clinical or safety data and further analyses of existing preclinical, clinical or safety data; that preclinical and clinical trial data are subject to differing interpretations and assessments, including during the peer review/publication process, in the scientific community generally, and by regulatory authorities; whether and when additional data from the BNT162 mRNA vaccine program will be published in scientific journal publications and, if so, when and with what modifications and interpretations; the expected time point for additional readouts on efficacy data of BNT162b2 or BNT162b5 in our clinical trials; the risk that more widespread use of the vaccine will lead to new information about efficacy, safety, or other developments, including the risk of additional adverse reactions, some of which may be serious; the nature of the clinical data, which is subject to ongoing peer review, regulatory review and market interpretation; whether and when submissions to request emergency use or any marketing approval for BNT162b5, BNT162b2 in additional populations, for a potential booster dose for BNT162b2, any monovalent, bivalent or variant-adapted vaccine candidates or any potential future vaccines (including potential future annual boosters or re-vaccination), and/or other biologics license and/or emergency use authorization applications or amendments to any such applications may be filed in particular jurisdictions for BNT162b5, BNT162b2, any monovalent or bivalent vaccine candidates or any other potential vaccines that may arise from the BNT162 program, including a potential variant-based, higher dose, or bivalent vaccine, and if obtained, whether or when such emergency use authorizations or licenses will expire or terminate; whether and when any applications that may be pending or filed for BNT162b2, BNT162b5, any monovalent, bivalent or variant-adapted vaccine candidates, or other vaccines that may result from the BNT162 program may be approved by particular regulatory authorities, which will depend on myriad factors, including making a determination as to whether the vaccines benefits outweigh its known risks and determination of the vaccines efficacy and, if approved, whether it will be commercially successful; our contemplated shipping and storage plan, including our estimated product shelf life at various temperatures; the ability of BioNTech to supply the quantities of BNT162, BNT162b5, any monovalent or bivalent vaccine candidates or any future vaccine, to support clinical development and market demand, including our production estimates for 2022; that demand for any products may be reduced or no longer exist which may lead to reduced revenues or excess inventory; the availability of raw materials to manufacture a vaccine; our vaccines formulation, dosing schedule and attendant storage, distribution and administration requirements, including risks related to storage and handling after delivery by Pfizer; the ability to successfully develop other vaccine formulations, booster doses or potential future annual boosters or re-vaccinations or new variant-based vaccines; the ability to maintain or scale up manufacturing capacity on a timely basis or maintain access to logistics or supply channels commensurate with global demand for our vaccine, which would negatively impact our ability to supply the estimated numbers of doses of our vaccine within the projected time periods as previously indicated; whether and when additional supply agreements will be reached; the ability to obtain recommendations from vaccine advisory or technical committees and other public health authorities and uncertainties regarding the commercial impact of any such recommendations; challenges related to public vaccine confidence or awareness; and uncertainties regarding the impact of COVID-19 on BioNTechs trials, business and general operations. Any forward-looking statements in this press release are based on BioNTech current expectations and beliefs of future events, and are subject to a number of risks and uncertainties that could cause actual results to differ materially and adversely from those set forth in or implied by such forward-looking statements. These risks and uncertainties include, but are not limited to: the ability to meet the pre-defined endpoints in clinical trials; competition to create a vaccine for COVID-19; the ability to produce comparable clinical or other results, including our stated rate of vaccine effectiveness and safety and tolerability profile observed to date, in the remainder of the trial or in larger, more diverse populations upon commercialization; the ability to effectively scale our productions capabilities; and other potential difficulties.For a discussion of these and other risks and uncertainties, see BioNTechs Annual Report as Form 20-F for the Year Ended December 31, 2021, filed with the SEC on March 30, 2022, which is available on the SECs website at http://www.sec.gov. All information in this press release is as of the date of the release, and BioNTech undertakes no duty to update this information unless required by law.

CONTACTS

Pfizer:Media Relations+1 (212) 733-7410[emailprotected]

Investor Relations+1 (212) 733-4848[emailprotected]

BioNTech:Media RelationsJasmina Alatovic+49 (0)6131 9084 1513[emailprotected]

Investor RelationsSylke Maas, Ph.D.+49 (0)6131 9084 1074[emailprotected]

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Pfizer and BioNTech Advance COVID-19 Vaccine Strategy With Study Start of Next-Generation Vaccine Candidate Based on Enhanced Spike Protein Design -...

By LAURA UNGAR

Two new studies provide more evidence that the coronavirus pandemic originated in a Wuhan, China market where live animals were sold further bolstering the theory that the virus emerged in the wild rather than escaping from a Chinese lab.

The research, published online Tuesday by the journal Science, shows that the Huanan Seafood Wholesale Market was likely the early epicenter of the scourge that has now killed nearly 6.4 million people around the world. Scientists conclude that the virus that causes COVID-19, SARS-CoV-2, likely spilled from animals into people two separate times.

All this evidence tells us the same thing: It points right to this particular market in the middle of Wuhan, said Kristian Andersen a professor in the Department of Immunology and Microbiology at Scripps Research and coauthor of one of the studies. I was quite convinced of the lab leak myself until we dove into this very carefully and looked at it much closer.

In one study, which incorporated data collected by Chinese scientists, University of Arizona evolutionary biologist Michael Worobey and his colleagues used mapping tools to estimate the locations of more than 150 of the earliest reported COVID-19 cases from December 2019. They also mapped cases from January and February 2020 using data from a social media app that had created a channel for people with COVID-19 to get help.

They asked, Of all the locations that the early cases could have lived, where did they live? And it turned out when we were able to look at this, there was this extraordinary pattern where the highest density of cases was both extremely near to and very centered on this market, Worobey said at a press briefing. Crucially, this applies both to all cases in December and also to cases with no known link to the market And this is an indication that the virus started spreading in people who worked at the market but then started to spread into the local community.

Andersen said they found case clusters inside the market, too, and that clustering is very, very specifically in the parts of the market" where they now know people were selling wildlife, such as raccoon dogs, that are susceptible to infection with the coronavirus.

In the other study, scientists analyzed the genomic diversity of the virus inside and outside of China starting with the earliest sample genomes in December 2019 and extending through mid-February 2020. They found that two lineages A and B marked the pandemics beginning in Wuhan. Study coauthor Joel Wertheim, a viral evolution expert at the University of California, San Diego, pointed out that lineage A is more genetically similar to bat coronaviruses, but lineage B appears to have begun spreading earlier in humans, particularly at the market.

Now I realize it sounds like I just said that a once-in-a-generation event happened twice in short succession, Wertheim said. But certain conditions were in place such as people and animals in close proximity and a virus that can spread from animals to people and from person to person. So barriers to spillover have been lowered such that multiple introductions, we believe, should actually be expected, he said.

Many scientists believe the virus jumped from bats to humans, either directly or through another animal. But in June, the World Health Organization recommended a deeper probe into whether a lab accident may be to blame. Critics had said the WHO was too quick to dismiss the lab leak theory.

Have we disproven the lab leak theory? No, we have not, Andersen said. But I think whats really important here is there are possible scenarios and there are plausible scenarios and its really important to understand that possible does not mean equally likely.

The pandemic's origins remain controversial. Some scientists believe a lab leak is more likely and others remain open to both possibilities. But Matthew Aliota, a researcher in the college of veterinary medicine at the University of Minnesota, said in his mind the pair of studies kind of puts to rest, hopefully, the lab leak hypothesis.

Both of these two studies really provide compelling evidence for the natural origin hypothesis," said Aliota, who wasn't involved in either study. Since sampling an animal that was at the market is impossible, "this is maybe as close to a smoking gun as you could get."

___

The Associated Press Health and Science Department receives support from the Howard Hughes Medical Institutes Department of Science Education. The AP is solely responsible for all content.

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New studies bolster theory coronavirus emerged from the wild - Daily Independent

If youre like most Americans, youve gotten your primary doses of a COVID-19 vaccine, but you havent gotten the recommended booster shots. So if its been several months since your last primary dose, youre probably due for a booster.

But the companies behind two of the more popular COVID-19 shots, Moderna and the team of Pfizer and BioNTech, have thrown a new variable into the mix. Last month, they said they had new versions of their booster shots that are designed to target the highly infectious Omicron family of COVID variants.

So you may be asking yourself, Should I get a booster shot now, while cases are surging, or should I wait until the new boosters are ready, probably this fall?

The answer, multiple vaccine experts said emphatically and without hesitation, is that theres no time like the present.

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Definitely get it now! Paula Cannon, a professor of molecular microbiology and immunology at USCs Keck School of Medicine, said in an email.

Trying to predict the future with this virus, even as close as the fall, is not a good idea, she said. And even with the more Omicron-specific vaccines, its still highly unlikely that they will provide absolute protection against infection.

That hardly makes them useless, Cannon noted: They will keep doing the much more important job that all the vaccines do, of protecting against severe illness and death.

The Centers for Disease Control and Prevention urges everyone whos at least 5 years old to get one to two booster shots, depending on their age and the health of their immune system. Thats because the protection offered by the vaccine fades over time.

But Dr. Thomas Campbell, an infectious disease specialist at the University of Colorado School of Medicine, said CDC data show that while two-thirds of the U.S. population has received the full course of primary doses (two shots in the case of Moderna and Pfizers vaccines, or one of the Johnson & Johnson vaccine), just under half of that group has gotten one booster shot. And less than 30% of the adults over 50 whove gotten one booster have gone on to receive the second recommended follow-up, Campbell said.

As a result, only a small percentage of the people across the population have received all the vaccine doses the CDC recommends, he said. Rather than waiting for the next generation of shots, Campbell said, people should get the boosters that theyre eligible for now.

He also noted that the forthcoming Moderna and Pfizer boosters, like the current ones, are available only to people who have received both of their primary doses. So if you stopped after one shot, you need to get the second one. Those shots provide certain forms of protection that the new boosters will not.

Dr. Otto Yang, professor of medicine and associate chief of infectious diseases at the David Geffen School of Medicine at UCLA, said the question of whether to wait for the new boosters has come up quite a lot, and that different people have different opinions. But his advice? Get it now, and then worry about the variant-specific booster later.

One major reason to get the shot now, he said, is the summer surge in reported cases. Another is that the current vaccine remains extremely good at keeping people from getting extremely ill or dying.

But a third reason, he said, is that the upside appears to be relatively small. Data from Moderna shows that its targeted booster was only modestly better than the current one in terms of antibody activity against Omicron.

And besides, antibodies are only part of the story when it comes to battling COVID.

Vaccines stimulate two different parts of the bodys immune system: antibodies, which mainly try to stop a virus from infecting a cell, and T cells, which can kill infected cells and stimulate the production of more antibodies. To oversimplify a bit, Yang said, antibodies seek to prevent an infection from spreading throughout your body, and if that fails, T cells try to prevent the infection from doing much damage.

The antibodies initially generated by the vaccine can prevent the coronavirus from latching on to healthy cells and fueling an infection. But SARS-CoV-2 has evolved, and variants like Omicron have changed enough that those antibodies may not recognize them.

Thats why the vaccines have not been very good at preventing people from getting infected by Omicron, Yang said. But the variant is about 97% the same as the original, he said, so the T cells stimulated by the vaccines arent hindered from doing their job.

Thats why the vaccines have continued to work very well in preventing us from getting [extremely] sick and dying, Yang said. And thats why the new vaccine is not going to be much better than the original, if at all, in preventing severe illness and death.

Research shows that vaccine-induced T cells fade over time, as do the antibodies. Thats why the CDC has recommended booster doses. At this point, the CDC is not recommending a second booster for people under 50 with healthy immune systems, or a third booster for people 50 and older or who are immunocompromised.

Many experts believe that annual or semi-annual COVID-19 boosters may ultimately be needed, but researchers are still studying the longer-term effectiveness of the vaccines.

The thing people have to realize, Campbell said, is that were learning how to use these vaccines as were using them.

One other X factor, according to Cannon, is the evolutionary path SARS-CoV-2 follows.

We dont even know that the virus variants circulating in the fall will still be Omicron and friends, she said. We could be looking at a completely new variant. ... So rather than trying to second-guess anything, we should stick with what we know, which is that boosters work well now, to top up peoples immunity.

The bottom line, Cannon said: If youre eligible for another dose, you should definitely go ahead and get a booster now.

About The Times Utility Journalism Team

This article is from The Times Utility Journalism Team. Our mission is to be essential to the lives of Southern Californians by publishing information that solves problems, answers questions and helps with decision making. We serve audiences in and around Los Angeles including current Times subscribers and diverse communities that havent historically had their needs met by our coverage.

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Should you wait for the Omicron booster? In a word, no - Los Angeles Times

Just 700 million years after the Big Bang, when the universe was still in its infancy, we already see supermassive black holes with the heft of 1 billion Suns. How could they have grown so fast? A team of astronomers is using computer simulations to glimpse what the formation of these dark behemoths might have looked like.

If you wish to make a billion-solar-mass black hole from scratch, to borrow a phrase, you must start with a star or perhaps only with the gas that stars are made of.

While the universes first stars might have made the first black holes, those would have been relatively small on the supermassive scale, with masses of only around 100 Suns. Perhaps the first stars clustered and so when stars made black holes, those black holes merged and then merged again. Even then, such black hole seeds would have been only 1,000, maybe 10,000 solar masses. These black holes would have had to grow super-fast to become supermassive in such a short amount of time.

But theres another way: Some astronomers have put forward the idea that in the small early universe, when gas was dense and pristine, gas clouds could collapse directly into more massive black holes.

The calculations for such massive implosions are delicate, though. Whats to prevent pieces of the gas cloud from cooling and collapsing under their own weight, as star-forming clouds in the modern universe are wont to do?

Some astronomers have suggested the ultraviolet emission of nearby newborn stars might have heated the gas, keeping it too warm to fragment. Others have argued that such specific requirements would make the process too rare to explain the number of supermassive black holes weve already found in the young universe.

Now, Muhammed Latif (United Arab Emirates University), Daniel Whalen (Portsmouth University, UK, and University of Vienna), and colleagues report in Nature that massive black holes can form without these special conditions.

The finding relies on computer simulations, which rebuild the conditions of the infant universe, when it was less than 100 million years old. Simulations are necessary because this era of the first stars is out of reach for our current telescopes.

The simulation followed the growth of a small, frothing sea of matter fed by four torrents of inflowing gas. While such nodes would have been common in the web of material filling the universe, Whalen says these streams were unusual because they carried so much gas. Latif adds that the rivers of gas were not only dense but fast-flowing; rushing in at speeds of 50 km/s (more than 100,000 mph), they carried between 1 and 10 Suns worth of material per year.

The sea at the center of these streams of material grew, and within the sea a clump took shape, and then another. The turbulence of inrushing gas flows kept the massive clumps from collapsing straightaway into stars; instead, the clumps continued to grow. By the end of the simulation 1.4 million years later they contained tens of thousands of Suns worth of mass.

Eventually, these clumps compress into what the researchers call supermassive stars; following their evolution requires a different kind of computer simulation, one that takes stellar physics into account. The stellar monstrosities dont last long in this simulation, just 1 million years, before they collapse again into black holes of 30,000 and 40,000 solar masses, respectively.

Such massive seeds could easily collect more gas and grow to become the dark behemoths seen by astronomers. Even though the kind of confluence explored in this study is rare, Latif, Whalen, and colleagues estimate that it would occur often enough to explain observations.

The new environment replete with cold flows thats numerically explored in this study is very exciting, says Priya Natarajan (Yale), as it seems to provide a natural pathway for the formation of massive black hole seeds.

But it isnt the only scenario that results in direct collapse, she cautions. Natarajan, who wasnt involved in the current study, explored a different scenario back in 2014, finding that a dense star cluster could similarly allow direct collapse to happen. The upshot isthat there are multiple pathways to rapidly amplifyand make massive black hole seeds in situ and early in the universe.

Upcoming James Webb Space Telescope observations, she adds, will help distinguish between the different black hole seed scenarios. Webb wont be able to detect the supermassive stars, even though theyre millions of times more luminous than the Sun, but its possible it could detect the black hole seeds that are still growing when the universe is less than 200 million years old.

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Where Did the First Quasars Come From? - Sky & Telescope - Sky & Telescope

Researchers have discovered the fastest star in the known universe.

The star, called S4716, orbits the Sagittarius A black hole in the centre of our Milky Way, located at a distance of 100 AU the distance between the Earth and the Sun from our planet.

The star is packed in an S cluster of over 100 stars known for moving particularly fast.

After observing S4716 for almost 20 years, the scientists have established that it travels around the supermassive black hole, which has a diameter of 23.5 million kilometers, in only four years at a speed of 8,000 kilometres per second.

For a star to be in a stable orbit so close and fast in the vicinity of a supermassive black hole was completely unexpected and marks the limit that can be observed with traditional telescopes, said Dr Florian Peissker, lead author of the new study.

The close-range orbit of S4716 is still puzzling to scientists. Stars cannot form so easily near the black hole. S4716 had to move inwards, for example by approaching other stars and objects in the S cluster, which caused its orbit to shrink significantly, Michael Zajaek, an astrophysicist at Masaryk University in Brno, Czech Republic, who was involved in the study, said.

A total of five telescopes were needed to observe the star, with four of these five being combined into one large telescope to allow even more accurate and detailed observations.

The researchwas published in The Astrophysical Journal.

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Astronomers discover the fastest star in the known universe - The Independent