Tag Archives: The Conversation

‘Mistaken, misread, misquoted, mislabeled, and mis-spoken’ – what Woody Guthrie wrote about the national debt debate in Congress during the Depression

The debt ceiling debate between the House GOP and President Joe Biden could, if not solved, lead to economic chaos and destruction – so it might seem strangely lighthearted to wonder what a Great Depression-era singer and activist would think about this particular political moment.

Certainly, in all the research I did in putting together my book “Prophet Singer: The Voice and Vision of Woody Guthrie,” I never came across any comment Woody Guthrie made about the debt ceiling.

But he lived through the Great Depression and its aftermath. He also stood witness to legislators struggling to correct the direction that the nation was headed in during the 1930s and early ‘40s.

He had a lot to say about Congress in general and how it handled the national debt in particular.

He once made a folksy joke that suggests his feelings about this supposedly august body.

“The Housewives of the country are always afraid at nite, afraid they’s a Robber in the House. Nope, Milady most of em is in the Senate,” he wrote in his regular column for The People’s Daily, called “Woody Sez.”

Guthrie constantly railed against politicians, both Republican and Democrat, who he thought represented their own selfish interests rather than those of deserving working men and women.

What if he could survey today’s America? Would his comments on the state of the nation in the past suggest that he would have something to say in 2023?

In fact, some of his observations sound as if they were written about this political moment – rather than his own.

When Guthrie visited Washington, D.C., in 1940, he managed to hear some Senate debates and provided his thoughts on their effectiveness.

“I gawthered the Reactionary Republicans was in love with the Reactionary Republicans; also that the Liberal Democrats was in love with th’ Liberal Demacrats. Each presented a brief case of statistics proving that the other brief cases of statistics, was mistaken, misread, misquoted, mislabeled, and mis-spoken,” he wrote in his column.

And just what were politicians arguing over then? The national debt.

Bipartisan legislative efforts raised the debt ceiling three times under President Donald Trump. Now, House Republicans are balking unless certain conditions are met, while the Democrats are demanding a clean bill with no restrictions.

Guthrie witnessed much the same situation in his era. During his visit to Washington, D.C., he listened to “senators a making speeches – on every conceivable subject under the sun, an’ though the manner in which they brought forth their arguments, their polished wit, and subtle maneuvers, were all very entertaining, I come out of it as empty handed as I went in,” he wrote in “Woody Sez.”

He then compared their debates to “hearin’ the hens a cacklin’ – and a runnin’ out to th barn.” Despite the scene’s being “loud, noisy, and plenty entertaining,” the result was “no eggs.”

There’s a lot of noise coming from Congress today also – but no results.

What could happen if the two sides cannot agree? A telling example occurred in 2011, when the bipartisan deal to raise the debt ceiling came so late that Standard & Poor’s downgraded the country’s credit rating – which hiked the interest that needed to be paid on the U.S. debt.

But if an agreement does not happen, Treasury Secretary Janet Yellen has warned that such a crisis would bring on “economic and financial catastrophe” on a national and global scale.

Guthrie would find this kind of brinkmanship troubling. Not because he was a political operative, with merely an intellectual understanding of the risks. Instead, he was driven by a personal knowledge of the day-to-day hardships, the human toll of such momentous political decisions. His family had fallen from middle-class safety into abject poverty even before the onset of the Great Depression.

Because of falling agricultural prices in the aftermath of World War I and his father’s real estate speculation in some small farms surrounding their hometown of Okemah, Oklahoma, the Guthries could not keep up with their mortgages. They were forced into foreclosure.

Guthrie joked that his father “was the only man in the world that lost a farm a day for thirty days.”

Foreclosures would likely be just one of the ruinous effects of default now, along with interest rates hikes, slashing of social programs, unemployment spikes and decimation of pension plans. All are negative results, but they are certain to hit the poor and working class the hardest.

Those are the people whom Woody Guthrie advocated for throughout his career. Those are the people whose hardships he lamented in such songs as “I Ain’t Got No Home” and “Dust Bowl Refugee.”

But he also expressed optimism about the power of those same people to make a positive change, such as in “Union Maid” and “Better World A-Comin’.” Individual and collective action was necessary, according to Guthrie, and he celebrated both. The union maid would “always get her way when she asked for better pay,” and in “Better World” he sings, “we’ll all be union and we’ll all be free.”

Perhaps his best-known comments about the nation appear in “This Land Is Your Land,” with the popular version praising the American landscape. But in his early version of that song, he ended it with his narrator surveying a line of hungry people lined up “by the relief office” and then asked, “Was this land made for you and me?”

That question could rise again in 2023: If congressional leaders debating over the debt ceiling fail to find common ground for the nation’s greater good, perhaps someone will challenge them and ask if the politicians are in office for the American people, or for themselves – just as Woody Guthrie would have.

Mark Allan Jackson

The Conversation

Vaccines using mRNA can protect farm animals against diseases traditional ones may not – and there are safeguards to ensure they won’t end up in your food

While effective vaccines for COVID-19 should have heralded the benefits of mRNA vaccines, fear and misinformation about their supposed dangers circulated at the same time. These misconceptions about mRNA vaccines have recently spilled over into worries about whether their use in agricultural animals could expose people to components of the vaccine within animal products such as meat or milk.

In fact, a number of states are drafting or considering legislation outlawing the use of mRNA vaccines in food animals or, at minimum, requiring their labeling on animal products in grocery stores. Idaho introduced a bill that would make it a misdemeanor to administer any type of mRNA vaccine to any person or mammal, including COVID-19 vaccines. A Missouri bill would have required the labeling of animal products derived from animals administered mRNA vaccines but failed to get out of committee. Arizona and Tennessee have also proposed labeling bills. Several other state legislatures are discussing similar measures.

I am a researcher who has been making vaccines for a number of years, and I started studying mRNA vaccines before the pandemic started. My research on using mRNA vaccines for cattle respiratory viruses has been referenced by social media users and anti-vaccine activists who say that using these vaccines in animals will endanger the health of people who eat them.

But these vaccines have been shown to reduce disease on farms, and it’s all but impossible for them to end up in your food.

In food animals, several types of vaccines have long been available for farmers to protect their animals from common diseases. These include inactivated vaccines that contain a killed version of a pathogen, live attenuated vaccines that contain a weakened version of a pathogen and subunit vaccines that contain one part of a pathogen. All can elicit good levels of protection from disease symptoms and infection. Producing these vaccines is often inexpensive.

However, each of these vaccines has drawbacks.

Inactivated and subunit vaccines often do not produce a strong enough immune response, and pathogens can quickly mutate into variants that limit vaccine effectiveness. The weakened pathogens in live attenuated vaccines have the remote possibility of reverting back to their full pathogenic form or mixing with other circulating pathogens and becoming new vaccine-resistant ones. They also must be grown in specific cell cultures to produce them, which can be time-consuming.

There are also several pathogens – such as porcine reproductive and respiratory syndrome virus, foot and mouth disease virus, H5N1 influenza and African swine fever virus – for which all three traditional approaches have yet to yield an effective vaccine.

Another major drawback for all three of these vaccine types is the time it takes to test and obtain federal approval to use them. Typically, animal vaccines take three or more years from development to licensure by the U.S. Department of Agriculture. Should new viruses make it to farms, playing catch-up using traditional vaccines could take too long to contain an outbreak.

All cells use mRNA, which contains the instructions to make the proteins needed to carry out specific functions. The mRNA used in vaccines encode instructions to make a protein from a pathogen of interest that immune cells learn to recognize and attack. This process builds immunological memory, so that when a pathogen carrying that same protein enters the body, the immune system will be ready to mount a quick and strong response against it.

Compared to traditional vaccines, mRNA vaccines have several advantages that make them ideal for protecting people and farm animals from both emerging and persistent diseases.

Unlike killed or subunit vaccines, mRNA vaccines increase the buildup of vaccine proteins in cells over time and train the immune system using conditions that look more like a viral infection. Like live attenuated vaccines, this process fosters the development of strong immune responses that may build better protection. In contrast to live attenuated viruses, mRNA vaccines cannot revert to a pathogenic form or mix with circulating pathogens. Furthermore, once the genetic sequence of a pathogen of interest is known, mRNA vaccines can be produced rather quickly.

The mRNA in vaccines can come in either a form that is structurally similar to what is normally found in the body, like those used in COVID-19 vaccines for people, or in a form that is self-amplifying, called saRNA. Because saRNA allows for higher levels of protein synthesis, researchers think that less mRNA would be needed to generate similar levels of immunity. However, a COVID-19 saRNA vaccine for people developed by biopharmaceutical company CureVac elicited less protection than traditional mRNA approaches.

Merck’s Sequivity is currently the only saRNA vaccine licensed for use in animals, and it is available by prescription to protect against swine flu in pigs.

All mRNA vaccines are made in the laboratory using methods that were developed decades ago. Only recently has the technology advanced to the point where the body doesn’t immediately reject it by activating the antiviral defenses intrinsic to each of your cells. This rejection would occur before the immune system even had the chance to mount a response.

The COVID-19 mRNA vaccines used in people mix in modified nucleotides – the building blocks of RNA – with unmodified nucleotides so the mRNA can hide from the intrinsic antiviral sensors of the cell. These modified nucleotides are what allow the mRNA to persist in the body’s cells for a few days rather than just a few hours like natural mRNAs.

New methods of delivering the vaccine using lipid nanoparticles also ensure the mRNA isn’t degraded before it has a chance to enter cells and start making proteins.

Despite this stability, mRNA vaccines do not last long enough within animals after injection for any component of the vaccine to end up on grocery store shelves. Unlike for human vaccines, animal vaccine manufacturers must determine the withdrawal period in order to obtain USDA approval. This means any component of a vaccine cannot be found in the animal prior to milking or slaughter. Given the short lifespan of some of the agriculture animals and intensive milking schedules, withdrawal periods often need to be very short.

Between the mandatory vaccine withdrawal period, flash pasteurization for milk, degradation on the shelf and the cooking process for food products, there could not be any residual vaccine left for humans to consume. Even if you were to consume residual mRNA molecules, your gastrointestinal tract will rapidly degrade them.

Several mRNA vaccines for use in animals are in early stages of development. Merck’s USDA-licensed Sequivity does not use the modified nucleotides or lipid nanoparticles that allow those vaccine components to circulate for slightly longer periods in the body, so long-term persistence is unlikely.

Like in people, animal vaccines are tested for their safety and effectiveness in clinical trials. Approval for use from the USDA Center for Vaccine Biologics requires a modest level of protection against infection or disease symptoms. As with all animal vaccines, future mRNA vaccines will also need to be fully cleared from the animal’s body before they can be used in animals for human consumption.

Whether mRNA vaccines will displace other vaccine types for livestock is yet to be determined. The cost of manufacturing these vaccines, their need to kept very cold and warm up before use to avoid degradation, and the efficacy of different types of mRNA vaccines all still need to be addressed before large-scale use can take place.

Traditional vaccines for food animals have protected them against many diseases. Limiting the use of mRNA vaccines right now would mean losing a new way to protect animals from pesky pathogens that current vaccines can’t fend off.

David Verhoeven

The Conversation

Pivotal points in the COVID-19 pandemic – 5 essential reads

Experts have made it clear that the end of the COVID-19 national emergency, which was lifted on May 11, 2023, does not mean an end to the pandemic. But this shift signals a remarkable turning point in a pandemic that is well into its fourth year – something that few could have imagined when the U.S. national emergency went into effect in March 2020.

Likewise, the World Health Organization’s announcement on May 5 that it was ending the COVID-19 public health emergency of international concern that had been in place since January 2020 is indicative that the pandemic has entered a new chapter.

It’s daunting to look back at our coverage and narrow it down to just a handful of standout stories amid all the twists and turns of the pandemic. But here are five stories from The Conversation’s archives that resonated with us, written by scholars who helped to illuminate complex issues at pivotal moments in the pandemic.

It’s a little hard to remember the days when words like pandemic, endemic diseases, mRNA, variant and spike proteins were not a part of our vernacular or everyday conversations. But I vividly recall the day that the COVID-19 pandemic was declared and a friend asked me “What exactly is a pandemic?” It turns out a lot of people were asking that question and wondering about the difference between an outbreak of an infectious disease, an epidemic and a pandemic.

Rebecca S.B. Fischer, an assistant professor of epidemiology at Texas A&M University, put it in straightforward terms: An outbreak is a small but unusual increase in the expected number of cases of a given disease, while the term epidemic is used when an infectious disease outbreak is getting bigger and spreading over a broader geographic area. A pandemic, on the other hand, is used when a disease is “international and out of control.”

She went on to say that some epidemiologists reserve the term pandemic for when a disease is being sustained in newly affected regions through local transmission – a good characterization of the state of COVID-19 in March 2020.

Read more:
What’s the difference between pandemic, epidemic and outbreak?

From the earliest days of the COVID-19 pandemic, it was impossible to miss the haunting similarities between it and the 1918 flu pandemic, which led to at least 50 million deaths worldwide between 1918 and 1920. Health care experts and the media made frequent comparisons between the two, pointing to similarities in attitudes about mask-wearing and school closures as well as in the patterns of disease waves, spikes and surges.

But while the two once-in-a-century events have shared plenty of likenesses, the comparison also sometimes led to public misunderstandings about how the COVID-19 pandemic could play out, wrote historian Mari Webel and pediatric infectious disease specialist Megan Culler Freeman, both from the University of Pittsburgh. They explain that key differences in the sociopolitical context of the 1918 flu period, as well as marked differences between the virology behind the two diseases, set the 1918 flu and COVID-19 on different paths.

“People seek answers from the experiences of influenza in 1918-19 for a fundamental reason: It ended.”

Read more:
Compare the flu pandemic of 1918 and COVID-19 with caution – the past is not a prediction

In late 2020, people were naturally wondering when and how the COVID-19 pandemic would end, and how we would know it was over.

Nükhet Varlik, a historian from Rutgers University who studies disease, medicine and public health, wrote an astute piece in October 2020 about the difficulties of predicting how the pandemic might play out. She presciently noted that “whether bacterial, viral or parasitic, virtually every disease pathogen that has affected people over the last several thousand years is still with us, because it is nearly impossible to fully eradicate them.” These include diseases like tuberculosis, leprosy, measles and plague.

“Hopefully COVID-19 will not persist for millennia,” Varlik wrote. But she went on to say that politics are crucial, noting how when vaccination programs are weakened, infections can “come roaring back.”

“Given such historical and contemporary precedents, humanity can only hope that the coronavirus that causes COVID-19 will prove to be a tractable and eradicable pathogen. But the history of pandemics teaches us to expect otherwise.”

Read more:
How do pandemics end? History suggests diseases fade but are almost never truly gone

The summer of 2021 felt like a particularly grueling moment in time – when excitement and optimism over the launch of the first vaccines to protect against COVID-19 had given way to despair over the stronghold of vaccine resistance and general exhaustion with all things COVID. And then came the delta variant.

Epidemiologist Katelyn Jetelina from the University of Texas Health Science Center at Houston captured 18 months of the COVID-19 pandemic in a series of seven retrospective charts that put all of the high and low points into stark relief. “The race between vaccination and variant spread was upon us,” Jetelina wrote. “The fight was far from over.”

The same may still be true today.

Read more:
18 months of the COVID-19 pandemic – a retrospective in 7 charts

When the omicron variant arrived on the scene in late 2021 and spread globally in early 2022, it soon became clear that it could bring about a shift in the pandemic. With its ability to spread easily and to also cause milder disease than prior variants, omicron had the potential to act as a natural vaccine of sorts – producing widespread immunity with the help of the existing COVID-19 vaccines.

But the omicron variant had plenty of surprises in store. For one, it gave rise to a family of variants and sublineages that to this day are keeping researchers guessing, with the latest omicron subvariant, XBB.1.16, gaining ground across the U.S. and worldwide as of mid-May 2023.

In January 2022, immunology researchers Prakash Nagarkatti and Mitzi Nagarkatti, from the University of South Carolina, explained how the immune system responds to infections and how it remembers those threats through “immunological memory.”

This left room for hope, they wrote, that “when new variants of SARS-CoV-2 inevitably arise, omicron will have left the population better equipped to fight them. So the COVID-19 vaccines combined with the omicron variant could feasibly move the world to a new stage in the pandemic – one where the virus doesn’t dominate our lives and where hospitalization and death are far less common.”

Read more:
Is the omicron variant Mother Nature’s way of vaccinating the masses and curbing the pandemic?

Editor’s note: This story is a roundup of articles from The Conversation’s archives.

Amanda Mascarelli

Katelyn Jetelina

Mari Webel

Megan Culler Freeman

Mitzi Nagarkatti

Nükhet Varlik

Prakash Nagarkatti

Rebecca S.B. Fischer

The Conversation

Passport bottleneck is holding up international travel by Americans eager to see the world as COVID-19 eases

The World Health Organization declared on May 5, 2023, that the COVID-19 pandemic is no longer a public health emergency. Although the virus is still causing hospitalizations and deaths, many travelers who were reluctant to go abroad because of the pandemic now feel freer to travel internationally again.

That’s going to be a whole lot easier to do this summer if you already have a valid passport. The wait times for getting one are soaring. The State Department says it can take up to 13 weeks for it to process passport applications, and up to nine weeks for expedited service that requires the payment of extra fees. It’s getting about 500,000 passport applications a week, which is at least 30% more than last year, Secretary of State Antony Blinken said in March. And delays in processing were already aggravating in 2021 and 2022.

I’m among the many Americans who have had to cancel or delay trips because of the long wait times. I was hoping to fly to London for a weeklong break between teaching economics courses. Unfortunately, renewing my passport took so long I couldn’t go.

The government says staffing issues are contributing to the delays. As an economist who researches the everyday experiences of consumers, I wondered if there was more to the story, since international travel is a big business. U.S. residents spent around US$17 billion in just the month of March 2023 going abroad.

Passports have been around a long time. They became more widespread about four centuries ago during the reign of the French King Louis the XIV. The king gave people with royal connections letters asking foreign officials to let the traveler “passe port” – French for pass through – the port or border of another country safely.

You can find a similar statement in the front of every U.S. passport, which “requests all whom it may concern to permit the citizen/national of the United States named herein to pass without delay or hindrance.”

One reason for the passport bottleneck in the United States is a long-term increase in demand for those official blue booklets. Back in 1989, there were three valid passports for every 100 people in this country. Today there are more than 45 passports for every 100 Americans. More recently, many Americans who let their passports expire because they were avoiding international travel when the pandemic began are eager to travel again.

The U.S. population has increased about 1% each year over the past three decades. During that same period the number of people holding a valid passport has jumped an average of 10% each year, 10 times faster than population growth.

Part of the rising demand for passports followed a policy change in the early 2000s. Before then no passport was required for U.S. citizens to travel to Canada, Mexico or the Caribbean. A driver’s license or an official document like a birth certificate was suitable documentation to visit countries that shared a common border with the U.S. By 2009, however, a passport was needed to visit those nearby countries by air, land or sea.

But the new rules don’t fully account for the surge in passport issuance. In 2010, about 100 million people had valid U.S. passports. Today, over 150 million do.

Another reason for the passport boom is that the State Department is fielding more requests than before for reissued passports to replace lost or stolen documents.

One problem while traveling is keeping your passport safe. While so far no one has ever stolen my passport, I have spilled food on it while climbing mountains, gotten it soaked in a monsoon and crushed it in my luggage on the world’s longest flight.

If your passport is ever lost, destroyed or stolen, you need to file a DS-64 form with the State Department. Filing this form prevents a thief from using that passport. The data is not just kept in the U.S. but is also sent to Interpol’s Stolen/Lost Travel Document database, which prevents worldwide travel by someone posing as you when traveling with your stolen passport.

The government periodically releases the number of DS-64 forms filed. In 2005 a bit more than 100,000 were submitted. This jumped fivefold to over 500,000 people who reported losing their passports in 2021.

Where do passport applications come from?

Not surprisingly, states with more people tend to get more passports. For example, Californians got the highest number of passports, about 2.7 million, in 2022.

But some states have more wanderlust than others. After adjusting for population, over the past few years the top two sources for international travel are the high-income states of New Jersey and Massachusetts. Around 1 out every 17 residents in those places applied annually for a passport.

The states where residents are the least likely to apply for a passport are the low-income states of Mississippi and West Virginia. In those places only about 1 out every 65 residents applied on average each year.

One of the reasons passport processing times have gotten so long is that many people are taking trips they put off in the spring of 2020. What can be done?

I suggest two things.

First, the Caribbean is one of the most popular U.S. tourist destinations. U.S. travelers today can visit the U.S. Virgin Islands and Puerto Rico without a passport because they are U.S. territories. I believe that expanding this access to a small number of Caribbean countries, as was possible before the 2009 policy change, would boost tourism and reduce passport demand.

Second, citizens with a current passport should be able to use it while waiting for a renewal. Right now old passports must be submitted with renewal forms, which blocks international travel. The State Department doesn’t really need the old documents. It recently ran a trial allowing people to renew passports online without asking for their current passport books.

Once a new passport is issued, the old one becomes invalid. This could present a problem for people traveling abroad while their passport renews. There is a simple solution for this. At the beginning of the COVID-19 pandemic the State Department allowed U.S. citizens who were abroad when their passports expired to reenter the country.

Extending this policy would mean people could continue traveling no matter how long it takes to renew their passport.

Jay L. Zagorsky

The Conversation

Many people are tired of grappling with long COVID – here are some evidence-based ways to counter it

A patient of mine, once a marathon runner, now gets tired just walking around the block. She developed COVID-19 during the 2020 Christmas holiday and saw me during the summer of 2021. Previously, her primary care doctor had recommended a graded exercise program. But exercise exhausted her. After months of waiting, she finally had an appointment at our post-COVID-19 clinic at the University of Virginia.

She is hardly alone in her extended search for answers. Studies suggest that from 10% to 45% of COVID-19 survivors have at least one of the following symptoms three months after recovery: fatigue, cough, shortness of breath, difficulty sleeping, difficulty with daily activities or mental fogginess, otherwise known as “brain fog.”

There are many names for this condition: long COVID, long-haul COVID, post-acute COVID-19 syndrome and chronic COVID. Patients report that their symptoms, or the severity of them, fluctuate over time, which makes diagnosis and treatment difficult.

Researchers and doctors have seen similar recovery patterns from other viruses, including Ebola and Middle East Respiratory Syndrome, or MERS, which is another coronavirus.

This suggests that the illness we see following a bout with COVID-19 may be part of a patient’s response to the infection. But doctors and researchers do not yet know why some patients go on to have persistent symptoms.

My clinical practice and academic research focus on critically ill patients. Most of my patients now are people who had COVID-19 with various levels of severity.

I often tell these patients that we are still learning about this disease, which wasn’t part of our vernacular before 2020. Part of what we do at the clinic is help patients understand what they can do at home to start improving.

Chronic fatigue can greatly affect quality of life. Exercise limitations can have their roots in problems with the lung, heart, brain, muscles or all of the above.

Graded exercise therapy works for some but not all patients. Graded exercise is the slow introduction of exercise, starting slowly and gradually increasing in load over time. Many are frustrated because they feel more exhausted after exercising or even doing the routine tasks of daily living. The lack of progress leads to feelings of depression.

The condition of feeling more exhausted after exercise is called post-exertional malaise, which is defined as physical and mental exhaustion after an activity, often 24 hours later, that is out of proportion with the activity.

For example, you feel good today and decide to go for a walk around the block. Afterward you are fine, but the next day your muscles ache and all you can do is lie on the couch. Some patients don’t even have the energy to answer emails. Rest or sleep do typically relieve the fatigue. There is no one-size-fits-all approach to treatment; the severity and frequency of post-exertional malaise varies from person to person.

Fatigue following any illness is common, as is exercise intolerance. So when should you see a medical professional? Diagnostic testing for post-exertional malaise exists, but it’s not readily available to all patients. These questions may provide clues to whether or not you are experiencing it:

All of these can be clues to discuss with your primary care provider, who may want to do additional testing to confirm the diagnosis, such as a two-day cardiopulmonary exercise test.

Before your appointment, there are a few things you can do at home that may help.

One of those techniques is pacing, or activity management, an approach that balances activities with rest.

The Royal College of Occupational Therapists and the Intensive Care Society, both in the U.K., developed what they call the 3Ps – Pace, Plan and Prioritize.

Pacing yourself means breaking down activities into smaller stretches with frequent breaks rather than doing it all at once. An example would be to climb a few steps and then rest for 30 seconds, instead of climbing all the stairs at once.

Planning involves looking at the week’s activities to see how they can be spread out. Think about the ones that are particularly strenuous, and give yourself extra time to complete them.

This helps with prioritizing – and recognizing those tasks that can be skipped or put off.

Some patients with long COVID develop abnormal breathing patterns, including shallow rapid breathing, known as hyperventilating, or breath-holding. Either of these patterns can make you feel short of breath.

Symptoms of abnormal breathing patterns include frequent yawning, throat-clearing, experiencing pins-and-needles sensations, palpitations and chest pain. Don’t ignore these symptoms, because they can be signs of serious medical problems like heart attacks and abnormal heart rhythms. Once those are ruled out, it is possible to relearn to breathe properly.

You can practice these techniques at home. The simple version: Find a comfortable position – either lying down or sitting upright with your back supported. Place one hand on your chest and the other over your belly button. Exhale any stale air out of your lungs. Then breathe in through your nose and into your abdomen, creating a gentle rise in the belly.

You should feel the hand resting on your belly button move up and down. Try to avoid short, shallow breaths into the upper chest. Slowly exhale all the air out of your lungs. The goal is to take around eight to 12 breaths per minute.

Focus on a longer exhale than inhale. For example, inhale as described for a count of two, then exhale for a count of three, as a starting point. If you take one breath every five seconds, you will be breathing 12 breaths per minute. As you get more comfortable with this, you can increase the time to further reduce your breaths per minute.

A more advanced tool is called box breathing: Breathe in for a count of four to five, holding your breath for a count of four to five, breathing out for a count of four to five and hold that for a count of four to five.

Long COVID patients who use these techniques show improvement in symptoms of breathlessness and sense of well-being.

The patient I referred to earlier did all of these things. As we worked with her, we discovered she had multiple reasons for her symptoms. In addition to overbreathing and symptoms of post-exertion malaise, she had a new cardiac problem, possibly related to her COVID-19 illness, that made her heart work less well during exercise. Now she is recovering; while not back to marathon running, she is feeling better.

Currently there is no cure for long COVID, though we hope research will lead to one. Clinical trials looking at potential therapies are continuing. In the meantime, people should be cautious about using medications that are not proved to help – and if you’re having symptoms, get evaluated.

Kyle B. Enfield

The Conversation

Cardiologists Explain Risks of Myocarditis From COVID Vaccines vs Risks of Heart Damage From Infection

What the research shows about risks of myocarditis from COVID vaccines versus risks of heart damage from COVID – two pediatric cardiologists explain how to parse the data.

Rare cases of myocarditis have been reported after COVID-19 vaccination, but the risk is higher after infection, and the prognosis is better following vaccine-related myocarditis. The decision to vaccinate should consider factors like patient age, health problems, and community COVID-19 rates.

Soon after the first COVID-19 vaccines appeared in 2021, reports of rare cases of heart inflammation, or myocarditis, began to surface.

In most instances, the myocarditis has been mild and responded well to treatment, though up to four potentially mRNA vaccine-related deaths from myocarditis in adults have been reported worldwide. No known verified deaths of children have been reported based on publicly available data. The exact number remains a topic of very heated debate because of variability in the reporting of possible myocarditis-related deaths.

Studies have largely confirmed that the overall myocarditis risk is significantly higher after an actual COVID-19 infection compared with vaccination, and that the prognosis following myocarditis due to the vaccine is better than from infection. The specific myocarditis risk varies by age and has been debated because of differing views among a small group of physicians related to risk tolerance and support for or against COVID-19 immunization for specific age groups.

As pediatric cardiologists, we specialize in heart issues relevant to kids of all ages. We believe it is important to weigh the risk of myocarditis caused by COVID-19 immunization against not only viral myocarditis from COVID-19, but also all the other complications that COVID-19 can lead to.

Comparing risks of myocarditis from severe disease versus COVID-19 vaccination or infection is difficult to do well, and debate continues over which of those outcomes poses a higher risk.

Myocarditis is any condition that causes heart inflammation. A closely related condition called pericarditis refers to inflammation of the outside lining of the heart. For the purpose of this article, we focus primarily on myocarditis, since it has the potential for being a more severe condition. Most cases of myocarditis are caused by infections, particularly viral ones.

Myocarditis can be confirmed by a combination of an electrocardiogram, an ultrasound heart picture called an echocardiogram, and some blood testing. When it is available, cardiac magnetic resonance imaging, or MRI, is the most accurate method to diagnose myocarditis that doesn’t involve an invasive procedure.

A mistaken assumption is that all myocarditis is severe, since it implies damage to the heart. However, mild cases in which there is very little swelling and only temporary damage to the heart are more common than severe cases that require a machine to support heart function.

Symptoms of myocarditis include chest pain and shortness of breath.

The challenge of parsing risks of myocarditis from viral infection compared with COVID-19 vaccination is due in part to the difficulty of establishing a diagnosis of myocarditis and its population rates accurately.

The United States Vaccine Adverse Event Reporting System, or VAERS – which is an initial reporting system for vaccine side effects – is by itself inadequate to determine the rate of any vaccine-associated side effect. This is because any side effect can be reported, and verification of a reported event only takes place afterward by the Centers for Disease Control and Prevention.

That vetted data is then reported in more robust databases like the Vaccine Safety Datalink. A very small number of the myocarditis events following COVID-19 vaccination have resulted in significant long-term consequences like heart rhythm troubles. However, such cases do not reflect the majority.

Thankfully, severe myocarditis after mRNA vaccination for COVID-19 is extremely rare. A 2021 study from Nordic scholars, which looked at comparative risks of myocarditis and heart arrhythmia in patients who experienced myocarditis after COVID-19 infection versus immunization found that the risks vary significantly by age group.

This has been touted as a reason not to vaccinate healthy young men against COVID-19. The follow-up study, however, found that the comparative risks of negative outcomes were worse from myocarditis from COVID-19 infection and other viral myocarditis than from vaccination in all patients older than 12 years of age.

And it’s worth noting that, as of mid-March 2023, the U.S. still leads the world in COVID-19 hospitalizations.

There have also been rare myocarditis cases reported with the newer non-mRNA Novovax vaccine, though we researchers do not yet know population-level rates.

A survey of all currently available research reveals that the risk of myocarditis after COVID-19 vaccination is highest in young men between the ages of 18 and 39 and older teen boys in the age range of 12 to 17, with the highest risk after the second dose of vaccine. The cause appears to be related to how the immune system processes the mRNA and sometimes generates an excessive immune response.

Myocarditis risk related to COVID-19 immunization is markedly lower in children younger than 12 years of age and much lower in adult males older than 50. The risk of severe disease from COVID-19, particularly in those older than 50 years, has been far higher throughout the pandemic than the risk of myocarditis from COVID-19 vaccination. The risk of vaccination myocarditis is uniformly lower in girls than in boys.

Infants younger than 6 months can get immunity only from their mother’s antibodies unless they are exposed to COVID-19 themselves, as vaccines for this age group are not available.

While the risks of myocarditis have been highest in teen boys and young men regardless of cause, the severity and outcome of myocarditis was much worse at the 90-day mark when it stemmed from COVID-19 infection or other viral diseases. This mirrors our team’s research on this same topic.

This discussion also doesn’t take into account the clot and heart attack risks from COVID-19 itself. Because COVID-19 damages blood vessels in all parts of the body, some organ damage such as kidney failure, blood clots, heart attacks and strokes can occur.

We recognize a need for more research into how people fare over the medium and long terms following a case of immunization-related myocarditis. This is why research is ongoing, and researchers like us are committed to following the data for years to come.

While there have been far fewer deaths from COVID-19 in children than adults, COVID-19 is still one of the leading causes of childhood death in the U.S., based on an early 2023 study. But COVID-19 deaths are not the only relevant measure of its effect in kids. COVID-19 has also killed more children in a shorter time period than several other vaccine-preventable diseases, such as hepatitis A and meningitis before the availability of their vaccines.

The argument that some have made that fewer children than adults die from COVID-19, or that it is often mild in children, has never been an acceptable justification to not do everything possible to protect children from it. For instance, doctors don’t stop treating pediatric cancer patients purely because there are fewer of them than adult cancer patients. And we don’t retire the measles vaccines only because most kids who get measles get only a mild case.

The primary risk that COVID-19 presents now to children is long COVID, followed by the risk of severe disease. The estimated percentage of children acquiring long COVID is still being debated, but the symptoms from long COVID can be extraordinarily debilitating. These include severe fatigue, brain fog, sleep disturbance, dizziness, nerve pain and more.

Many children with long COVID-19 report lingering fatigue and frequent headaches.

We believe that the decision of whether to vaccinate against COVID-19 should be based upon the patient’s age, other health problems, relative risk from vaccines, how much and what type of COVID-19 is in your community, and the patient’s and family’s preference.

Two ways that have been suggested by the CDC and the Public Health Agency of Canada to decrease the risk of COVID-19 vaccine myocarditis are to opt for Pfizer and to space your doses out by at least eight weeks. This is because Pfizer has slightly lower rates of myocarditis than Moderna.

Adults who are immunocompromised or have other medical problems known to worsen COVID-19 disease severity still carry the highest risk of severe disease. They should therefore follow the CDC COVID-19 vaccination schedule with additional boosters, if advised by their physician.

While COVID-19 immunizations are not as efficient at preventing viral transmission now as they were with the earliest variant, they remain highly effective at reducing severe illness and hospitalization, even in kids, and particularly in the high-risk state of pregnancy.

Thankfully kids have fared far better from COVID-19 infection than adults. The primary risks of severe COVID-19 for children are among babies and infants, as well as children with health problems that put them at high risk, children with the most significant types of congenital heart disease or those with other medically complex conditions. Children in those groups derive the most benefit from the primary COVID-19 vaccine series; therefore, the decision to vaccinate in their case should be easier.

Informed consent that comes with vaccination should involve discussion of infection risks. The risk of immunization will never be zero because of variability in immune system responses; therefore, making the decision should always involve considering the most-up-to date information available.

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This article was first published in The Conversation.The Conversation

Reconstructing ancient bacterial genomes can revive previously unknown molecules – offering a potential source for new antibiotics

Microorganisms – in particular bacteria – are skillful chemists that can produce an impressive diversity of chemical compounds known as natural products. These metabolites provide the microbes major evolutionary advantages, such as allowing them to interact with one another or their environment and helping defend against different threats. Because of the diverse functions bacterial natural products have, many have been used as medical treatments such as antibiotics and anti-cancer drugs.

The microbial species alive today represent only a tiny fraction of the vast diversity of microbes that have inhabited Earth over the past 3 billion years. Exploring this microbial past presents exciting opportunities to recover some of their lost chemistry.

Directly studying these metabolites in archaeological samples is virtually impossible because of their poor preservation over time. However, reconstructing them using the genetic blueprints of long-dead microbes could provide a path forward.

We are a team of anthropologists, archaeogeneticists and biochemists who study ancient microbes. By generating previously unknown chemical compounds from the reconstructed genomes of ancient bacteria, our newly published research provides a proof of concept for the potential use of fossil microbes as a source of new drugs.

The cellular machinery producing bacterial natural products is encoded in genes that are typically in close proximity to one another, forming what are called biosynthetic gene clusters. Such genes are difficult to detect and reconstruct from ancient DNA because very old genetic material breaks down over time, fragmenting into thousands or even millions of pieces. The end result is numerous tiny DNA fragments less than 50 nucleotides long all mixed together like a jumbled jigsaw puzzle.

We sequenced billions of such ancient DNA fragments, then improved a bioinformatic process called de novo assembly to digitally order the ancient DNA fragments in stretches of up to 100,000 nucleotides long – a 2,000-fold improvement. This process allowed us to identify not only what genes were present, but also their order in the genome and the ways they differ from bacterial genes known today – key information to uncovering their evolutionary history and function.

This method allowed us to take an unprecedented look at the genomes of microbes living up to 100,000 years ago, including species not known to exist today. Our findings push back the previously oldest reconstructed microbial genomes by more than 90,000 years.

In the microbial genomes we reconstructed from DNA extracted from ancient tooth tartar, we found a gene cluster that was shared by a high proportion of Neanderthals and anatomically modern humans living during the Middle and Upper Paleolithic that lasted from 300,000 to 12,000 years ago. This cluster bore the molecular hallmarks of very ancient DNA and belonged to the bacterial genus Chlorobium, a group of green sulfur bacteria capable of photosynthesis.

We inserted a synthetic version of this gene cluster into a “modern” bacterium called Pseudomona protegens so it could produce the chemical compounds encoded in the ancient genes. Using this method, we were able to isolate two previously unknown compounds we named paleofuran A and B and determine their chemical structure. Resynthesizing these molecules in the lab from scratch confirmed their structure and allowed us to produce larger quantities for further analysis.

By reconstructing these ancient compounds, our findings highlight how archaeological samples could serve as new sources of natural products.

Microbes are constantly evolving and adapting to their surrounding environment. Because the environments they inhabit today differ from those of their ancestors, microbes today likely produce different natural products than ancient microbes from tens of thousands of years ago.

As recently as 25,000 to 10,000 years ago, the Earth underwent a major climate shift as it transitioned from the colder and more volatile Pleistocene Epoch to the warmer and more temperate Holocene Epoch. Human lifestyles also dramatically changed over this transition as people began living outside of caves and increasingly experimented with food production. These changes brought them into contact with different microbes through agriculture, animal husbandry and their new built environments. Studying Pleistocene-era bacteria may yield insights into bacterial species and biosynthetic genes no longer associated with humans today, and perhaps even microbes that have gone extinct.

While the amount of data collected by scientists on biological organisms has exponentially increased over the past few decades, the number of new antibiotics has stagnated. This is particularly problematic when bacteria are able to evade existing antibiotic treatments faster than researchers can develop new ones.

By reconstructing microbial genomes from archaeological samples, scientists can tap into the hidden diversity of natural products that would have otherwise been lost over time, increasing the number of potential sources from which they can discover new drugs.

Our study has shown that it is possible to access natural products from the past. To tap into the vast diversity of chemical compounds encoded in ancient DNA, we now need to streamline our methodology to be less labor-intensive.

We are currently optimizing and automating our process to identify biosynthetic genes in ancient DNA more quickly and reliably. We are also implementing robotic liquid handling systems to complete the time-consuming pipetting and bacterial cultivation steps in our methods. Our goal is to scale up the process to be able to translate a vast amount of data on ancient microbes into the discovery of new therapeutic agents.

Although we can recreate ancient molecules, their biological and ecological roles are difficult to decipher. Since the bacteria that originally produced these compounds no longer exist, we cannot culture or genetically manipulate them. Further study will need to rely on similar bacteria that can be found today. Whether or not the functions of these compounds have remained the same in the modern relatives of ancient microbes remains to be tested. Although the original functions of these compounds for ancient microbes may be unknown, they still have the potential to be repurposed to treat modern diseases.

Ultimately, we aim to shed new light on microbial evolution and fight the current antibiotic crisis by providing a new time axis for antibiotic discovery.

Christina Warinner

Alexander Hübner

Pierre Stallforth

The Conversation

How do Candida auris and other fungi develop drug resistance? A microbiologist explains

One of the scariest things you can be told when at a doctor’s office is “You have an antimicrobial-resistant infection.” That means the bacteria or fungus making you sick can’t be easily killed with common antibiotics or antifungals, making treatment more challenging. You might have to take a combination of drugs for weeks to overcome the infection, which could result in more severe side effects.

Unfortunately, this diagnosis is becoming more common around the world.

The yeast Candida auris has recently emerged as a potentially dangerous fungal infection for hospital patients and nursing home residents. First discovered in the late 2000s, Candida auris has very quickly become a major health challenge due to its ease of spread and ability to resist common antifungal drugs.

How did this fungus become so strong, and what can researchers and physicians do to combat it?

I am a microbiologist researching new ways to kill fungi. Candida auris and other fungi use three common cellular tricks to overcome treatments. Luckily, exciting new research hints at ways we can still fight this fungus.

Fungal cells contain a structure called a cell wall that helps maintain their shape and protects them from the environment. Fungal cell walls are constructed in part from several different types of polysaccharides, which are long strings of sugar molecules linked together.

Two polysaccharides found in almost all fungal cell walls are chitin and beta-glucan. The fungal cell wall is an attractive target for drugs because human cells do not have a cell wall, so drugs that block chitin and beta-glucan production will have fewer side effects.

Some of the most common drugs used to treat fungal infections are called echinocandins. These drugs stop fungal cells from making beta-glucan, which significantly weakens their cell wall. This means the fungal cell can’t maintain its shape well. While the fungus is struggling to grow or is breaking apart, your immune system has a much better chance of fighting off the infection.

Unfortunately, some strains of Candida auris are resistant to echinocandin treatment. But how does the fungus actually do it? For decades, scientists have been studying how fungi overcome drugs designed to weaken or kill them. In the case of echinocandins, Candida auris commonly uses three tricks to beat these treatments: hide, build and change.

The first trick is to hide in a complex mixture of sugars, proteins, DNA and cells called a biofilm. Made with irregular 3D structures, biofilms have lots of places for cells to hide. Drugs aren’t good at penetrating biofilms, so they can’t access and kill cells deep inside. Biofilms are especially problematic when they grow on medical equipment like ventilators or catheters. Once free of a biofilm, cells that have gained the ability to resist the drugs a patient was taking become more dangerous.

The second trick fungi use to evade treatment is to build cell walls differently. Fungal cells treated with echinocandins can’t make beta-glucan. So instead, they start to make more chitin, another important polysaccharide in the fungal cell wall. Echinocandins are unable to stop chitin production, so the fungus is still able to build a strong cell wall and avoid being killed. While there are some drugs that can stop chitin production, none are currently approved for use in people.

The third trick fungi rely on is to change the shape of the beta-glucan production enzyme so echinocandins cannot block it. These mutations allow beta-glucan production to continue even in the presence of the drug. It is not surprising that Candida uses this trick to resist antifungal drugs since it is very effective at keeping the cells alive.

What can be done to treat echinocandin-resistant fungal infections? Thankfully, scientists and physicians are researching new ways to kill Candida auris and similar fungi.

The first approach is to find new drugs. For example, there are two drugs in development, rezafungin and ibrexafungerp, that appear to be able to stop beta-glucan production even in fungi resistant to echinocandins.

A complementary approach my research group is exploring is whether a class of enzymes called glycoside hydrolases might also be able to combat drug-resistant fungi. Some of these enzymes actively destroy the fungal cell wall, breaking apart both beta-glucan and chitin at the same time, which could potentially help prevent fungi from surviving on medical equipment or on hospital surfaces.

My lab’s work on discovering enzymes that strongly degrade fungal cell walls is part of a new strategy to combat antifungal resistance that uses a combination of approaches to kill fungi. But the end goal of this research is the same: having a physician tell you, “You’ve got a fungal infection, but we have a good treatment for it now.”

Jeffrey Gardner

The Conversation

Here’s why your freezer smells so bad – and what you can do about it

Most people would expect a freezer can keep perishable food fresh and safe from spoilage for many months. Unfortunately, this is not always the case.

Have you ever noticed a funky smell in your freezer? Where does it come from and what can be done to fix the problem?

There are several causes for bad smells coming from your freezer. Typically, the culprits are microbes – bacteria, yeasts and moulds.

Although a freezer dramatically slows down the growth of most common spoilage microbes, some can still thrive if the temperature rises above -18℃ (the recommended freezer temperature). This can happen if there is a power outage for more than a few hours, or if you put something hot straight in the freezer.

Food spills and open containers provide an opportunity for microbes to get to work. It’s also worth noting that many microbes will survive freezing and start growing again once conditions are favourable – for example, if you remove the food, partially thaw it, and return it to the freezer.

Two things happen when food breaks down. First, as microbes start to grow, several pungent chemicals are produced. Second, the fats and flavours that are part of the food itself can and will be released.

These are generally referred to as volatile organic compounds (VOCs). They are the pleasant aromas that we sense when we eat, but VOCs can also be produced by bacteria.

For example, many of us would be familiar with the smells that come from fermentation – a microbial process. When fermenting a food, we intentionally contaminate it with microbes of known characteristics, or provide conditions that favour the growth of desirable microbes and subsequent production of aromatic compounds.

By contrast, uncontrolled food spoilage is problematic, especially when the contaminating microbes can cause disease.

It is not only microbial growth that can lead to undesirable odours. There’s a suite of chemical processes happening in the freezer, too.

Freezing causes physical changes to foods, often enhancing their breakdown. Many of us would be familiar with “freezer burn” on meats and other foods, as well as ice crystals on frozen food.

This phenomenon is called “salt rejection”. Depending on how rapidly something is frozen, salts can sometimes be concentrated, as pure water freezes at a higher temperature than water with things dissolved in it – like sugars and salts. On a large scale, this happens to icebergs in the ocean. As the sea water freezes, salt is removed. Thus, the iceberg is composed of fresh water, and the surrounding sea water becomes a saltier and denser brine.

In a similar way, as water in food freezes, organic molecules are concentrated and expelled. If these are volatile, they move about the freezer and stick to other things. Where they end up depends on what else is around.

Some of the volatiles like water. We call them “hydrophilic” or water loving; those are the ones that will make your food taste bad. Other are more water-hating or “hydrophobic” and they stick to things like silicone ice cube trays, making them go smelly.

Domestic freezers are commonly attached to a refrigerator, and this provides another opportunity for smells to move through the systems. The two units share a single cooling source and airflow channel. If your fridge has foul odours from the food inside (natural or after microbial spoilage), it is very likely they will migrate to your freezer.

Read more:
How colour-coding your fridge can stop your greens going to waste

There are some simple steps you can take to stop your freezer from smelling.

First, try to prevent odours from developing in the first place by covering the food. If you place food in an airtight container (glass is best), it will dramatically slow the release of any aromatic compounds produced by bacteria or the food itself. Covered food is also less likely to absorb smells and flavours from other foods around it.

If the smells have already developed, you can eliminate them by following a few simple steps, including a thorough clean.

If the smells are not removed with these simple cleaning steps, the freezer may require a deep clean, which involves turning off the unit and letting it “breathe” for a few days.

Placing some baking soda inside the freezer before adding food can help to absorb any residual odours. For serious smells where crevices or insulation are contaminated, you may need a service technician.

In short, even though we think freezers keep things “fresh”, microbes can still proliferate in there. Make sure to clean your freezer now and then to keep your food safe and healthy.

Enzo Palombo

Rosalie Hocking

The Conversation

Silent Epidemic: Oral Sex Is Now the Leading Risk Factor for Throat Cancer

The rapid rise in oropharyngeal cancer in the West over the past two decades is largely attributed to the sexually transmitted human papillomavirus (HPV). Despite the potential protective effect of HPV vaccinations, challenges such as vaccine hesitancy, low coverage in certain regions, and behavioral trends could undermine its effectiveness. While a gender-neutral vaccination policy has been introduced in several countries, achieving comprehensive disease control still presents significant obstacles.

Over the past two decades, there has been a rapid increase in throat cancer in the West, to the extent that some have called it an epidemic. This has been due to a large rise in a specific type of throat cancer called oropharyngeal cancer (the area of the tonsils and back of the throat). The main cause of this cancer is the human papillomavirus (HPV), which is also the main cause of cancer of the cervix. Oropharyngeal cancer has now become more common than cervical cancer in the US and the UK.

HPV is sexually transmitted. For oropharyngeal cancer, the main risk factor is the number of lifetime sexual partners, especially oral sex. Those with six or more lifetime oral-sex partners are 8.5 times more likely to develop oropharyngeal cancer than those who do not practice oral sex.

Behavioral trends studies show that oral sex is very prevalent in some countries. In a study that my colleagues and I conducted in almost 1,000 people having tonsillectomy for non-cancer reasons in the UK, 80% of adults reported practicing oral sex at some point in their lives. Yet, mercifully, only a small number of those people develop oropharyngeal cancer. Why that is, is not clear.

The prevailing theory is that most of us catch HPV infections and are able to clear them completely. However, a small number of people are not able to get rid of the infection, maybe due to a defect in a particular aspect of their immune system. In those patients, the virus is able to replicate continuously, and over time integrates at random positions into the host’s DNA, some of which can cause the host cells to become cancerous.

HPV vaccination of young girls has been implemented in many countries to prevent cervical cancer. There is now increasing, albeit as yet indirect evidence, that it may also be effective in preventing HPV infection in the mouth. There is also some evidence to suggest that boys are also protected by “herd immunity” in countries where there is high vaccine coverage in girls (over 85%). Taken together, this may hopefully lead in a few decades to the reduction of oropharyngeal cancer.

That is well and good from a public health point of view, but only if coverage among girls is high – over 85%, and only if one remains within the covered “herd.” It does not, however, guarantee protection at an individual level – and especially in this age of international travel – if, for example, someone has sex with someone from a country with low coverage. It certainly does not afford protection in countries where vaccine coverage of girls is low, for example, the US where only 54.3% of adolescents aged 13 to 15 years had received two or three HPV vaccination doses in 2020.

This has led several countries, including the UK, Australia, and the US, to extend their national recommendations for HPV vaccination to include young boys – called a gender-neutral vaccination policy.

But having a universal vaccination policy does not guarantee coverage. There is a significant proportion of some populations who are opposed to HPV vaccination due to concerns about safety, necessity, or, less commonly, due to concerns about encouraging promiscuity.

Paradoxically, there is some evidence from population studies that, possibly in an effort to abstain from penetrative intercourse, young adults may practice oral sex instead, at least initially.

The coronavirus pandemic has brought its own challenges, too. First, reaching young people at schools was not possible for a period of time. Second, there has been an increasing trend in general vaccine hesitancy, or “anti-vax” attitudes, in many countries, which may also contribute to a reduction in vaccine uptake.

As always when dealing with populations and behavior, nothing is simple or straightforward.

Written by Hisham Mehanna, Professor, Institute of Cancer and Genomic Sciences, University of Birmingham.

This article was first published in The Conversation.The Conversation