Health

2022 was the year many people decided the coronavirus pandemic had ended.

President Joe Biden said as much in an interview with 60 Minutes in September. “The pandemic is over,” he said while strolling around the Detroit Auto Show. “We still have a problem with COVID. We’re still doing a lot of work on it. But the pandemic is over.”

His evidence? “No one’s wearing masks. Everybody seems to be in pretty good shape.”

But the week Biden’s remarks aired, about 360 people were still dying each day from COVID-19 in the United States. Globally, about 10,000 deaths were recorded every week. That’s “10,000 too many, when most of these deaths could be prevented,” the World Health Organization Director-General Tedros Adhanom Ghebreyesus said in a news briefing at the time. Then, of course, there are the millions who are still dealing with lingering symptoms long after an infection.
Those staggering numbers have stopped alarming people, maybe because those stats came on the heels of two years of mind-boggling death counts (SN Online: 5/18/22). Indifference to the mounting death toll may reflect pandemic fatigue that settled deep within the public psyche, leaving many feeling over and done with safety precautions.

“We didn’t warn people about fatigue,” says Theresa Chapple-McGruder, an epidemiologist in the Chicago area. “We didn’t warn people about the fact that pandemics can last long and that we still need people to be willing to care about yourselves, your neighbors, your community.”

Public health agencies around the world, including in Singapore and the United Kingdom, reinforced the idea that we could “return to normal” by learning to “live with COVID.” The U.S. Centers for Disease Control and Prevention’s guidelines raised the threshold for case counts that would trigger masking (SN Online: 3/3/22). The agency also shortened suggested isolation times for infected people to five days, even though most people still test positive for the virus and are potentially infectious to others for several days longer (SN Online: 8/19/22).

The shifting guidelines bred confusion and put the onus for deciding when to mask, test and stay home on individuals. In essence, the strategy shifted from public health — protecting your community — to individual health — protecting yourself.
Doing your part can be exhausting, says Eric Kennedy, a sociologist specializing in disaster management at York University in Toronto. “Public health is saying, ‘Hey, you have to make the right choices every single moment of your life.’ Of course, people are going to get tired with that.”

Doing the right thing — from getting vaccinated to wearing masks indoors — didn’t always feel like it paid off on a personal level. As good as the vaccines are at keeping people from becoming severely ill or dying of COVID-19, they were not as effective at protecting against infection. This year, many people who tried hard to make safe choices and had avoided COVID-19 got infected by wily omicron variants (SN Online: 4/22/22). People sometimes got reinfected — some more than once (SN: 7/16/22 & 7/30/22, p. 8).
Those infections may have contributed to a sense of futility. “Like, ‘I did my best. And even with all of that work, I still got it. So why should I try?’ ” says Kennedy, head of a Canadian project monitoring the sociological effects of the COVID-19 pandemic.

Getting vaccinated, masking and getting drugs or antibody treatments can reduce the severity of infection and may cut the chances of infecting others. “We should have been talking about this as a community health issue and not a personal health issue,” Chapple-McGruder says. “We also don’t talk about the fact that our uptake [of these tools] is nowhere near what we need” to avoid the hundreds of daily deaths.

A lack of data about how widely the coronavirus is still circulating makes it difficult to say whether the pandemic is ending. In the United States, the influx of home tests was “a blessing and a curse,” says Beth Blauer, data lead for the Johns Hopkins University Coronavirus Resource Center. The tests gave an instant readout that told people whether they were infected and should isolate. But because those results were rarely reported to public health officials, true numbers of cases became difficult to gauge, creating a big data gap (SN Online: 5/27/22).
The flow of COVID-19 data from many state and local agencies also slowed to a trickle. In October, even the CDC began reporting cases and deaths weekly instead of daily. Altogether, undercounting of the coronavirus’s reach became worse than ever.

“We’re being told, ‘it’s up to you now to decide what to do,’ ” Blauer says, “but the data is not in place to be able to inform real-time decision making.”

With COVID-19 fatigue so widespread, businesses, governments and other institutions have to find ways to step up and do their part, Kennedy says. For instance, requiring better ventilation and filtration in public buildings could clean up indoor air and reduce the chance of spreading many respiratory infections, along with COVID-19. That’s a behind-the-scenes intervention that individuals don’t have to waste mental energy worrying about, he says.

The bottom line: People may have stopped worrying about COVID-19, but the virus isn’t done with us yet. “We have spent two-and-a-half years in a long, dark tunnel, and we are just beginning to glimpse the light at the end of that tunnel. But it is still a long way off,” WHO’s Tedros said. “The tunnel is still dark, with many obstacles that could trip us up if we don’t take care.” If the virus makes a resurgence, will we see it coming and will we have the energy to combat it again?

A group at the National Bureau of Standards at B­oulder, Colo., now reports an extremely accurate [speed of light] measurement using the wavelength and frequency of a helium-neon laser.… The result gives the speed of light as 299,792.4562 kilometers per second.

Update
That 1972 experiment measured the two-way speed of light, or the average speed of photons that traveled from their source to a reflective surface and back. The result, which still holds up, helped scientists redefine the standard length of the meter (SN: 10/22/83, p. 263). But they weren’t done putting light through its paces. In the late 1990s and early 2000s, photons set a record for slowest measured speed of light at 17 meters per second and froze in their tracks for one-thousandth of a second (SN: 1/27/01, p. 52). For all that success, one major hurdle remains: directly testing the one-way speed of light. The measurement, which many scientists say is impossible to make, could resolve the long-standing question of whether the speed of light is uniform in all directions.

Some immune defenses of the brain may have their roots in the gut.

A new study in mice finds that immune cells are first trained in the gut to recognize and launch attacks on pathogens, and then migrate to the brain’s surface to protect it, researchers report online November 4 in Nature. These cells were also found in surgically removed parts of human brains.

Every minute, around 750 milliliters of blood flow through the brain, giving bacteria, viruses or other blood-borne pathogens an opportunity to infect the organ. For the most part, the invaders are kept out by three membrane layers, called the meninges, which wrap around the brain and spinal cord and act as a physical barrier. If a pathogen does manage to breach that barrier, the researchers say, the immune cells trained in the gut are ready to attack by producing a battalion of antibodies.

The most common route for a pathogen to end up in the bloodstream is from the gut. “So, it makes perfect sense for these [immune cells] to be educated, trained and selected to recognize things that are present in the gut,” says Menna Clatworthy, an immunologist at the University of Cambridge.

Clatworthy’s team found antibody-producing plasma cells in the leathery meninges, which lie between the brain and skull, in both mice and humans. These immune cells produced a class of antibodies called immunoglobulin A, or IgA.

These cells and antibodies are mainly found in the inner lining of the gut and lungs, so the scientists wondered if the cells on the brain had any link to the gut. It turned out that there was: Germ-free mice, which had no microbes in their guts, didn’t have any plasma cells in their meninges either. However, when bacteria from the poop of other mice and humans were transplanted into the mice’s intestines, their gut microbiomes were restored, and the plasma cells then appeared in the meninges.

“This was a powerful demonstration of how important the gut could be at determining what is found in the meninges,” Clatworthy says.

Researchers captured microscope images of an attack in the meninges of mice that was led by plasma cells that had likely been trained in the guts. When the team implanted a pathogenic fungus, commonly found in the intestine, into the mice’s bloodstream, the fungus attempted to enter the brain through the walls of blood vessels in the meninges. However, plasma cells in the membranes formed a mesh made of IgA antibodies around the pathogen, blocking its entry. The plasma cells are found along the blood vessels, Clatworthy says, where they can quickly launch an attack on pathogens.

“To my knowledge, this is the first time anyone has shown the presence of plasma cells in the meninges. The study has rewritten the paradigm of what we know about these plasma cells and how they play a critical role in keeping our brain healthy,” says Matthew Hepworth, an immunologist at the University of Manchester in England who was not involved with the study. More research is needed to classify how many of the plasma cells in the meninges come from the gut, he says.

The finding adds to growing evidence that gut microbes can play a role in brain diseases. A previous study, for instance, suggested that in mice, boosting a specific gut bacterium could help fight amyotrophic lateral sclerosis, or ALS, a fatal neurological disease that results in paralysis (SN: 7/22/19). And while the new study found the plasma cells in the brains of healthy mice, previous research has found other gut-trained cells in the brains of mice with multiple sclerosis, an autoimmune disease of the brain and the spinal cord.

For now, the researchers want to understand what cues plasma cells follow in the guts to know it is time for them to embark on a journey to the brain.

It’s official: 2020 now has the most named storms ever recorded in the Atlantic in a single year.

On November 9, a tropical disturbance brewing in the northeastern Atlantic Ocean gained enough strength to become a subtropical storm. With that, Theta became the year’s 29th named storm, topping the 28 that formed in 2005.

With maximum sustained winds near 110 kilometers per hour as of November 10, Theta is expected to churn over the open ocean for several days. It’s too early to predict Theta’s ultimate strength and trajectory, but forecasters with the National Oceanic and Atmospheric Administration say they expect the storm to weaken later in the week.

If so, like most of the storms this year, Theta likely won’t become a major hurricane. That track record might be the most surprising thing about this season — there’s been a record-breaking number of storms, but overall they’ve been relatively weak. Only five — Laura, Teddy, Delta, Epsilon and Eta — have become major hurricanes with winds topping 178 kilometers per hour, although only Laura and Eta made landfall near the peak of their strength as Category 4 storms.

Even so, the 2020 hurricane season started fast, with the first nine storms arriving earlier than ever before (SN: 9/7/20). And the season has turned out to be the most active since naming began in 1953, thanks to warmer-than-usual water in the Atlantic and the arrival of La Niña, a regularly-occurring period of cooling in the Pacific, which affects winds in the Atlantic and helps hurricanes form (SN: 9/21/19). If a swirling storm reaches wind speeds of 63 kilometers per hour, it gets a name from a list of 21 predetermined names. When that list runs out, the storm gets a Greek letter.

While the wind patterns and warm Atlantic water temperatures set the stage for the string of storms, it’s unclear if climate change is playing a role in the number of storms. As the climate warms, though, you would expect to see more of the destructive, high-category storms, says Kerry Emanuel, an atmospheric scientist at MIT. “And this year is not a poster child for that.” So far, no storm in 2020 has been stronger than a Category 4. The 2005 season had multiple Category 5 storms, including Hurricane Katrina (SN: 12/20/05).

There’s a lot amount of energy in the ocean and atmosphere this year, including the unusually warm water, says Emanuel. “The fuel supply could make a much stronger storm than we’ve seen,” says Emanuel, “so the question is: What prevents a lot of storms from living up to their potential?”
A major factor is wind shear, a change in the speed or direction of wind at different altitudes. Wind shear “doesn’t seem to have stopped a lot of storms from forming this year,” Emanuel says, “but it inhibits them from getting too intense.” Hurricanes can also create their own wind shear, so when multiple hurricanes form in close proximity, they can weaken each other, Emanuel says. And at times this year, several storms did occupy the Atlantic simultaneously — on September 14, five storms swirled at once.

It’s not clear if seeing hurricane season run into the Greek alphabet is a “new normal,” says Emanuel. The historical record, especially before the 1950s is spotty, he says, so it’s hard to put this year’s record-setting season into context. It’s possible that there were just as many storms before naming began in the ‘50s, but that only the big, destructive ones were recorded or noticed. Now, of course, forecasters have the technology to detect all of them, “so I wouldn’t get too bent out of shape about this season,” Emanuel says.

Some experts are hesitant to even use the term “new normal.”

“People talk about the ‘new normal,’ and I don’t think that is a good phrase,” says James Done, an atmospheric scientist at the National Center for Atmospheric Research in Boulder, Colo. “It implies some new stable state. We’re certainly not in a stable state — things are always changing.”

When some bacteria manage to escape being killed by a virus, the microbes end up hamstringing themselves. And that could be useful in the fight to treat infections.

The bacterium Shigella flexneri — one cause of the infectious disease shigellosis — can spread within cells that line the gut by propelling itself through the cells’ barriers. That causes tissue damage that can lead to symptoms like bloody diarrhea. But when S. flexneri in lab dishes evolved to elude a type of bacteria-killing virus, the bacteria couldn’t spread cell to cell anymore, making it less virulent, researchers report November 17 in Applied and Environmental Microbiology.

The research is a hopeful sign for what’s known as phage therapy (SN: 11/20/02). With antibiotic-resistant microbes on the rise, some researchers see viruses that infect and kill only bacteria, known as bacteriophages or just phages, as a potential option to treat antibiotic-resistant infections (SN: 11/13/19). With phage therapy, infected people are given doses of a particular phage, which kill off the problematic bacteria. The problem, though, is that over time those bacteria can evolve to be resistant against the phage, too.

“We’re kind of expecting phage therapy to fail, in a sense,” says Paul Turner, an evolutionary biologist and virologist at Yale University. “Bacteria are very good at evolving resistance to phages.”
But that doesn’t mean the bacteria emerge unscathed. Some phages attack and enter bacteria by latching onto bacterial proteins crucial for a microbe’s function. If phage therapy treatments relied on such a virus, that could push the bacteria to evolve in such a way that not only helps them escape the virus but also impairs their abilities and makes them less deadly. People infected with these altered bacteria might have less severe symptoms or may not show symptoms at all.

Previous studies with the bacteria Pseudomonas aeruginosa, for instance, have found that phage and bacteria can engage in evolutionary battles that drive the bacteria to be more sensitive to antibiotics. The new study hints that researchers could leverage the arms race between S. flexneri and the newly identified phage, which was dubbed A1-1 after being found in Mexican wastewater, to treat shigellosis.

S. flexneri in contaminated water is a huge problem in parts of the world where clean water isn’t always available, such as sub-Saharan Africa and southern Asia, says Kaitlyn Kortright, a microbiologist also at Yale University. Every year, approximately 1.3 million people die from shigellosis, which is caused by four Shigella species. More than half of those deaths are in children younger than 5 years old. What’s more, antibiotics to treat shigellosis can be expensive and hard to access in those places. And S. flexneri is becoming resistant to many antibiotics. Phage therapy could be a cheaper, more accessible option to treat the infection.

The blow to S. flexneri’s cellular spread comes because to enter cells, A1-1 targets a protein called OmpA, which is crucial for the bacteria to rupture host cell membranes. The researchers found two types of mutations that made S. flexneri resistant to A1-1. Some bacteria had mutations in the gene that produces OmpA, damaging the protein’s ability to help the microbes spread from cell to cell. Others had changes to a structural component of bacterial cells called lipopolysaccharide.

The mutations in lipopolysaccharide were surprising, Kortright says, because the relationship between that structural component and OmpA isn’t fully worked out. One possibility is that those mutations distort OmpA’s structure in a way that the phage no longer recognizes it and can’t enter bacterial cells.

One lingering question is whether S. flexneri evolves in the same way outside a lab dish, says Saima Aslam, an infectious diseases physician at the University of California, San Diego who was not involved in the work. Still, the findings show that it’s “not always a bad thing” when bacteria become phage-resistant, she says.

Regenerating body parts is never easy. For instance, some lizards can grow back their tails, but these new appendages are pale imitations of the original. Now, genetically modified stem cells are helping geckos grow back better tails.

Tweaking and implanting embryonic stem cells on the tail stumps of mourning geckos (Lepidodactylus lugubris) allowed the reptiles to grow tails that are more like the original than ever before, researchers report October 14 in Nature Communications. These findings are a stepping-stone to developing regenerative therapies in humans that may one day treat hard-to-heal wounds.

A gecko’s tail is an extension of its spine — with the vertebrae to prove it. Regenerated tails, however, are simpler affairs. “It’s just a bunch of concentric tubes of fat, muscle and skin,” says Thomas Lozito, a biologist at the University of Southern California in Los Angeles.

That’s because stem cells in adult geckos produce a molecular signal that encourages the formation of cartilage in new tails, but not bone or nervous tissues (SN: 8/17/18). Lozito and his colleagues used embryonic stem cells, which can develop into a wider range of tissues than adult stem cells, modified them to ignore this signal and then implanted them on the tail stumps of geckos that had their tails surgically removed. The tails that grew from these modified stem cells had bonelike grooves in the cartilage and generated new neural tissue at the top of the tail.

These modified tails still lack a spinal cord, making them a far cry from the original. “We fixed one problem, but there are still many imperfections,” Lozito says. “We’re still on the hunt for the perfect tail.”

A meandering trek taken by light from a remote supernova in the constellation Cetus may help researchers pin down how fast the universe expands — in another couple of decades.

About 10 billion years ago, a star exploded in a far-off galaxy named MRG-M0138. Some of the light from that explosion later encountered a gravitational lens, a cluster of galaxies whose gravity bent the light so that we see multiple images. In 2016, the supernova appeared in Earth’s sky as three distinct points of light, each marking three different paths the light took to get here.

Now, researchers predict that the supernova will appear again in the late 2030s. The time delay — the longest ever seen from a gravitationally lensed supernova — could provide a more precise estimate for the distance to the supernova’s host galaxy, the team reports September 13 in Nature Astronomy. And that, in turn, may let astronomers refine estimates of the Hubble constant, the parameter that describes how fast the universe expands.

The original three points of light appeared in images from the Hubble Space Telescope. “It was purely an accident,” says astronomer Steve Rodney of the University of South Carolina in Columbia. Three years later, when Hubble reobserved the galaxy, astronomer Gabriel Brammer at the University of Copenhagen discovered that all three points of light had vanished, indicating a supernova.
By calculating how the intervening cluster’s gravity alters the path the supernova’s light rays take, Rodney and his colleagues predict that the supernova will appear again in 2037, give or take a couple of years. Around that time, Hubble may burn up in the atmosphere, so Rodney’s team dubs the supernova “SN Requiem.”

“It’s a requiem for a dying star and a sort of elegy to the Hubble Space Telescope itself,” Rodney says. A fifth point of light, too faint to be seen, may also arrive around 2042, the team calculates.、
The predicted 21-year time delay — from 2016 to 2037 — is a record for a supernova. In contrast, the first gravitational lens ever found — twin images of a quasar spotted in 1979 — has a time delay of only 1.1 years (SN: 11/10/1979).

Not everyone agrees with Rodney’s forecast. “It is very difficult to predict what the time delay will be,” says Rudolph Schild, an astrophysicist at the Harvard-Smithsonian Center for Astrophysics in Cambridge, Mass., who was the first to measure the double quasar’s time delay. The distribution of dark matter in the galaxy hosting the supernova and the cluster splitting the supernova’s light is so uncertain, Schild says, that the next image of SN Requiem could come outside the years Rodney’s team has specified.

In any case, when the supernova image does appear, “that would be a phenomenally precise measurement” of the time delay, says Patrick Kelly, an astronomer at the University of Minnesota in Minneapolis who was not involved with the new work. That’s because the uncertainty in the time delay will be tiny compared with the tremendous length of the time delay itself.

That delay, coupled with an accurate description of how light rays weave through the galaxy cluster, could affect the debate over the Hubble constant. Numerically, the Hubble constant is the speed a distant galaxy recedes from us divided by the distance to that galaxy. For a given galaxy with a known speed, a larger estimated distance therefore leads to a lower number for the Hubble constant.

This number was once in dispute by a factor of two. Today the range is much tighter, from 67 to 73 kilometers per second per megaparsec. But that spread still leaves the universe’s age uncertain. The frequently quoted age of 13.8 billion years corresponds to a Hubble constant of 67.4. But if the Hubble constant is higher, then the universe could be about a billion years younger.

The longer it takes for SN Requiem to reappear, the farther from Earth the host galaxy is — which means a lower Hubble constant and an older universe. So if the debate over the Hubble constant persists into the 2030s, the exact date the supernova springs back to life could help resolve the dispute and nail down a fundamental cosmological parameter.

The complete field of 16 teams that will advance to the 2021-22 UEFA Champions League knockout rounds has not yet been finalized, but we already have several clubs that have booked their spots.

European giants Liverpool, Ajax, Bayern Munich and Juventus were the first four teams to clinch on Matchday 4 of the group stage, while Manchester United and Chelsea joined them on Matchday 5.
Only the top two teams in each group advance, and there's incentive to win the group when it comes to the Round of 16 draw on Monday, Dec. 13. The first-place team from each group will be seeded, and their Round of 16 opponent will be drawn from a pot of the second-place finishers.

Champions League Round of 16 qualifiers
Group 1st Place 2nd Place
Grp A — —
Grp B Liverpool —
Grp C Ajax —
Grp D — —
Grp E Bayern Munich —
Grp F Manchester United —
Grp G — —
Grp H Chelsea / Juventus Chelsea / Juventus
When is the Champions League Round of 16 draw?
The Round of 16 draw will be held on Dec. 13 at 6 a.m. ET from the UEFA headquarters in Switzerland. It will be streamed by UEFA.com.

The eight group winners will be seeded for purposes of the draw. They will make up one pot, while the other pot will contain the runners-up from each group.

The two key details to remember for this Round of 16 draw:

Teams from the same country cannot be drawn against one another (see table below);
The group winners (i.e. seeded teams) will host the second leg of each Round of 16 series. This is perceived to be an advantage because, if an extra-time session or penalty-kick shootout is needed, it would happen on home soil.
Knockout round qualifiers by country
Nation Total Clubs Clubs
England 3 Chelsea, Liverpool, Manchester United
Germany 1 Bayern Munich
Italy 1 Juventus
Netherlands 1 Ajax Amsterdam
The two legs of the Round of 16 will be spread over eight days between February and March. The second leg of each series will take place three weeks after the first leg.

The eight teams left standing will participate in a quarterfinal draw on March 18, 2022, which will determine the rest of the Champions League bracket through the final in Saint Petersburg on May 28. There are no seedings involved in this draw, and unlike the Round of 16, teams from the same country can be drawn against one another.

Champions League Round of 16 schedule
Round of 16, 1st Legs
Date Match Time (ET) TV channels Stream
Feb. 15 Round of 16 #1 3 p.m. TBD fuboTV, Paramount+
Feb. 15 Round of 16 #2 3 p.m. TBD fuboTV, Paramount+
Feb. 16 Round of 16 #3 3 p.m. TBD fuboTV, Paramount+
Feb. 16 Round of 16 #4 3 p.m. TBD fuboTV, Paramount+
Feb. 22 Round of 16 #5 3 p.m. TBD fuboTV, Paramount+
Feb. 22 Round of 16 #6 3 p.m. TBD fuboTV, Paramount+
Feb. 23 Round of 16 #7 3 p.m. TBD fuboTV, Paramount+
Feb. 23 Round of 16 #8 3 p.m. TBD fuboTV, Paramount+
Round of 16, 2nd Legs
Date Match Time (ET) TV channels Stream
March 8 Round of 16 #1 3 p.m. TBD fuboTV, Paramount+
March 8 Round of 16 #2 3 p.m. TBD fuboTV, Paramount+
March 9 Round of 16 #3 3 p.m. TBD fuboTV, Paramount+
March 9 Round of 16 #4 3 p.m. TBD fuboTV, Paramount+
March 15 Round of 16 #5 3 p.m. TBD fuboTV, Paramount+
March 15 Round of 16 #6 3 p.m. TBD fuboTV, Paramount+
March 16 Round of 16 #7 3 p.m. TBD fuboTV, Paramount+
March 16 Round of 16 #8 3 p.m. TBD fuboTV, Paramount+
Who will win the UEFA Champions League 2021-22?
As the tournament progresses, the oddsmakers are constantly adjusting the future prices for each team when it comes to winning the Champions League. Here are the latests odds courtesy of U.S.-based DraftKings (asterisk denotes teams that have already qualified for the Round of 16):

Champions League outright winner odds
Team Nov. 23
Manchester City +300
Bayern Munich* +350
PSG +500
Liverpool* +550
Chelsea* +600
Manchester United* +1200
Ajax* +2000
Real Madrid +2200
Atletico Madrid +3500
Juventus* +3500
Inter Milan +5000
B. Dortmund +5000
Barcelona +5000
Atalanta +10000
Porto +15000
Benfica +15000
Villarreal +15000
RB Salzburg +15000
Sevilla +20000
Wolfsburg +30000
Lille +50000
Club Brugge +80000
Sporting CP +100000
UEFA Champions League 2021-2022: Tournament format
The 2021-2022 edition of the UEFA Champions League features a familiar format — and one massive new twist.

As usual, the tournament started out with a group stage (eight groups of four teams each), and only the top two finishers in each group advance to the Round of 16 that kicks off in February 2022. Two-leg, aggregate-goal knockout rounds are played the rest of the way through to the single game final that will be held in Russia on May 28, 2022.

Group Stage: Sept. 14-15, Sept. 28-29, Oct. 19-20, Nov. 2-3, Nov. 23-24, Dec. 7-8
Round of 16: Feb. 15-16, March 8-9 / Feb. 22-23, March 15-16
Quarterfinals: April 5-6, April 12-13
Semifinals: April 26-27, May 3-4
Final: May 28, 2022 (St. Petersburg, Russia)
No away goals tiebreaker in Champions League
Here's that twist: For the first time since 1965, there will be no away goals tiebreaker used in the knockout rounds of UEFA competitions, including the Champions League, after it was abolished in June 2021.

Series that are tied on aggregate goals after the conclusion of the second leg will go straight to extra time and, if necessary, a penalty-kick shootout.

How to watch the UEFA Champions League
The 2021-22 UEFA Champions League will be carried in the United States by CBS (English) and Univision (Spanish) across a number of TV and streaming platforms.

CBS Sports will have live pregame, halftime and postgame studio shows, which will air on CBS Sports Network and stream on Paramount+. Also back this year is the RedZone-like whip-around show called "The Golazo Show," also on CBS Sports Network and Paramount+, with all the goals and best chances from the concurrent matches.

Univision will mirror that coverage with its own pregame and postgame shows. Its whip-around show is called "Zona Fútbol."

Nearly every Champions League match is available to be streamed on fuboTV, which offers a free seven-day trial to new subscribers. The streaming platform carries all the Univision family of channels: Univision, TUDN, UniMas, Galavision and TUDNxtra.

Univision will stream select matches on its ad-supported platform PrendeTV, which is available free of charge across mobile and connected TV devices, Amazon Fire TV, Apple (iOS and tvOS), Google (Android phones and TV devices), Roku, and via the web on Prende.tv.

There will be much more on the line Saturday night than just the WBO welterweight title.

If Terence Crawford can defeat Shawn Porter to move to 38-0, he could set himself up for even bigger battles down the road. Even Crawford himself has acknowledged that he has more blockbuster bouts on his mind, including a potential clash with Errol Spence Jr.
"I've been calling for these fights," Crawford told Timothy Bradley Jr. "Me and Shawn, we talked about fighting. I've told him, 'I'm not looking to fight you.' I'm looking to fight Spence. I'm looking to fight Keith Thurman because, you know, they got something to offer. I'm looking at them trying to use Shawn as a pawn because they know Shawn, he's gonna fight anybody.

"If I do too good, they might back up even more. We're here now. I'm gonna show them why they've been ducking me."

Can Crawford continue his run of dominance and put a notable win on his resume? Or will Porter pull off the upset in Las Vegas?
Boxing fans can purchase the Crawford vs. Porter pay-per-view through ESPN+. The prelim card will air live on ESPN2 starting at 7 p.m. ET.

What time is Terence Crawford vs. Shawn Porter?
Date: Saturday, Nov. 20
Time: 9 p.m. ET | 6 p.m. PT
Main event: 11:30 p.m. ET | 8:30 p.m. PT (estimate)
The Crawford vs. Porter fight card is scheduled to start at 9 p.m. ET on Saturday, Nov. 20. Crawford and Porter are expected to make their ring walks around 11:30 p.m. ET, though that could change depending on the length of the earlier fights.

Terence Crawford vs. Shawn Porter fight card
Terence Crawford vs. Shawn Porter for Crawford's WBO welterweight title
Esquiva Falcao vs. Patrice Volny; Middleweight
Janibek Alimkhanuly vs. Hassan N'Dam; Middleweight
Raymond Muratalla vs. Steven Ortiz; Lightweight
We may earn an affiliate commission when you sign up for a streaming service through our links. Sporting News' affiliates have no influence over the editorial content included in this article.

The Denver Nuggets will be without their superstar and the league's reigning MVP Nikola Jokic when they take on the Bulls at home.

This is the first game that Jokic will miss this season due to an injury, with the only other game he didn't suit up for so far was due to a suspension, following his altercation with the Miami Heat's Markieff Morris.
Through 14 games, he's averaging career-highs of 26.4 points and 13.6 rebounds while also dishing out 6.4 assists on career-high shooting efficiencies of 59.3 percent from the field and 41.0 percent from beyond the arc.
What's next for Jokic? Here's everything we know about his injury.

What is Nikola Jokic's injury?
Hours before the game against the Bulls, the Nuggets declared Jokic out with a right wrist sprain.
It's an injury that the Serbian big man reportedly suffered midway through the team's previous game, a home loss against the Philadelphia 76ers. Although he played until the end, he was seen favouring it in the second half.

How long is Nikola Jokic out?
It's currently unknown if Jokic will miss more than one game. In addition, the Nuggets will be without other key young stars in Jamal Murray (ACL) and Michael Porter Jr. (back).

The Serbian has been one of the most reliable players in his career, having missed just 20 games through his six previous seasons.

Nuggets upcoming schedule
The Nuggets enter this Bulls game with a 9-6 record, good for sixth in the West prior to Friday's games.

After this Bulls game, Denver will kick-off a road-heavy schedule as they play nine of their next 10 games away from home.

Date Opponent Time (ET)
Nov. 21 at Suns 8:00 p.m.
Nov. 23 at Trail Blazers 10:00 p.m
Nov. 26 vs. Bucks 9:00 p.m
Nov. 29 at Heat 7:30 p.m
Dec. 1 at Magic 7:00 p.m
Currently, the Nuggets rank third in defensive rating (103.8) and 20th in offensive rating (106.2).