Category: Health

Nothing puts a damper on a beautiful summer day like getting stung by a bee, wasp, hornet or yellowjacket (all of which we classify under the term “bee sting”). Fortunately, bee sting treatment is usually straightforward. Home remedies and some over-the-counter first aid items are typically all you need to care for your bee sting.

With the right steps and remedies, you can be back outside enjoying the sunshine in no time at all. Read on to learn what bee stings look like, what treatments can help and when to worry about allergic reactions.

Note: If you are having a severe allergic reaction (anaphylaxis), which can be characterized by swelling in your face and throat, fainting, nausea, difficulty breathing or loss of consciousness, call 911 to seek emergency treatment immediately.

What does a bee sting look like?

Most people know when they’ve been stung by a bee. It hurts. Plus, the culprit is usually nearby, or it left its stinger behind. But sometimes, all you know is that something stung or bit you. This is especially true for young children.

Toddlers may not have the skills to tell you what happened, but they sure can alert you to the place where it hurts. That’s why it’s important to know what a bee sting looks like. After all, you need to be sure you’re treating the right sting.

Your body can react in one of four ways to getting stung by a bee.

1. Local reactions – Local reactions are the most common. These stings will look like a bad mosquito bite. The area will be red, the center may be white and there may be a small brown stinger still in your skin. A welt may also form.
2. Large local reactions – Large local reactions are the second most common. They’re similar to local reactions, except the area of reaction around the bite tends to be bigger.
3. Toxic reactions – Toxic reactions are rare. They occur when your body has a toxic response to the venom in the stinger and you may feel nauseous or lightheaded.
4. Allergic/anaphylactic reactions– Anaphylactic reactions are very rare. This is when your body has a severe allergic response to the sting. If this occurs, you must call 911 to get emergency treatment immediately. We’ll explain the signs to look for below.

Most of us will experience a local or large local reaction to a bee sting. These are handily treated on your own with first aid and home remedies.

Bee sting swelling and pain

Bee stings hurt. Anyone who says otherwise is probably just trying to impress you. When you get stung by a bee, expect these common symptoms

• Pain:  It’s okay to admit that it hurts. A bee sting feels like a sharp poke, as if you’ve been jabbed with a needle unexpectedly.
• Swelling:  The affected area typically swells a little, sometimes a lot. If you were stung on your hands or fingers, be sure to remove any rings quickly. The swelling can make it hard to take rings off and could cause loss of circulation.
• Itchiness:  You might mistake your bee sting for a mosquito bite thanks to the itchiness it can cause.
• Burning:  Stings can burn to the point where there’s no mistaking it for anything other than a bee sting.

How to treat a bee sting

If your bee sting has caused a local reaction, there’s no need to seek medical care – you can treat it at home. You’ll first need to remove the stinger, if it’s there, and then focus on treating the sting. If you’re unsure of what to do at any step of the way, you can always call our nurse line for helpful tips and reassurance.

How to remover a stinger

Fun fact: One way to know what kind of insect stung you is to check for a stinger. If you’ve got one stuck in your skin, you were stung by a honeybee. A honeybee is the only species with a stinger that detaches, which means that the honeybee will sting and then die. On the other hand, wasps, hornets and other types of bees will fly off to sting again (and again and again).

A stinger will look like a small brown or black dot in the middle of your sting. It will have tiny barbs on it, keeping it lodged in your skin, and perhaps even a venom sac. Don’t worry about looking too closely, just try to get it out as quickly and completely as you can. You can use tweezers, your fingernails (only after you wash your hands), scrape the edge of a credit card across it, or even use sticky tape to remove the stinger. And if you don’t get all of it, it’s not the end of the world – the rest will come out naturally over a little time.

Home remedies for bee stings

There are a lot of ways to treat bee stings at home, and with items you probably have in your bathroom cabinet or kitchen first aid kit. One of the best things you can do to treat a bee sting at home is use a cold pack or an ice cube to massage the sting. Leave the cold on for 10 minutes at a time and repeat as needed. This will reduce the pain as well as the swelling.

Another home remedy that you could try is honey. Strangely enough, honey seems to soothe angry bee stings. When you consider that honey is often the base ingredient to many homemade drawing salves, there could be more to this treatment method than we give it credit for.

What about mud? Mud is a common home remedy, however mud contains a lot of germs and may even contain tetanus spores. It’s an unsafe home remedy that you should avoid.

If you’re looking for solutions that are more tested than the home remedies mentioned above, you’ve got options, including pain and allergy medications.

• For pain, you can take acetaminophen (Tylenol) or ibuprofen (Advil or Motrin). You should only have to take one dose of this as the pain should subside in a few hours. Be sure to use as directed.
• If the sting is bothering you because it continues to itch or burn, try hydrocortisone cream. This can be applied three times a day. For extra relief, you can put the cream in the refrigerator because cold is particularly soothing. You should only need to treat your bee sting for a few days with hydrocortisone cream, and no more than a week.
• Antihistamines such as cetirizine or loratadine (brand names include Reactine, Zyrtec and Claritin) are pills you can take once a day for moderate to severe itching. These also provide relief and are available as over-the-counter options at your neighborhood pharmacy or drugstore.

When does a bee sting get better?

You’ve done your best to treat your bee sting at home, followed all the advice and even consulted our nurse line to be sure you were on the right track. So, when can you expect this bee sting to get better? The short answer is 3-7 days. In that time, you will likely experience:

• Pain and burning for 1-2 hours. That should be the worst of it before it subsides. Don’t forget to use whatever home remedies or treatments work best for you.
• Redness and swelling for about 24 hours. Don’t be surprised if the swelling actually increases. That’s to be expected, as well as redness, as your body processes the venom.

Can bee stings get infected?

Rarely, through scratching or other outside irritation, a bee sting can become infected. An infected bee sting will have a gooey yellowish-brown crust or scab covering the top of it. The scab may weep or drain yellow fluid.

To treat an infected bee sting, be sure to keep it clean. This will help it get better at home.

• Wash the area with antibacterial soap and warm water.
• Remove any scab. Bacteria live under the scab. Soaking the scab with a warm wet washcloth can help.
• Pat dry and apply antibiotic ointment three times a day.
• Cover with a clean, dry bandage.

With this treatment, you can expect your infected bee sting to improve within 2-3 days and be completely healed within 7-10 days.

What to know for next time

Having been stung by a bee once, you’re undoubtedly motivated to not let it happen again. Here are a few quick tips for avoiding stings in the future:

• Wear long-sleeve shirts and long pants when you’re in grassy outdoor areas.
• Skip perfumes and hair products, as well as brightly colored clothes.
• Yellowjackets love the smell of food, so take care when cooking or eating outside.

Toxic and allergic reactions to bee stings

Very rarely, toxic and allergic reactions can occur when you’re stung by a bee. They’re both potentially life threatening, but can be effectively treated when caught early and in the right circumstances.

Toxic reactions to bee stings

A toxic reaction to a bee sting happens when a person has the very bad luck of getting stung multiple times. Someone who’s experiencing a toxic reaction may feel nauseous, vomit and develop diarrhea. Within 24 hours, muscle breakdown and renal failure may occur if left untreated. It’s estimated that around 500 stings are enough bee venom to cause death.

Anaphylaxis

Only 0.04% of the population will experience an anaphylactic reaction to a bee sting. It can happen with just one sting, and usually starts within 20 minutes. If you haven’t experienced symptoms within two hours, the chances of you developing anaphylaxis are slim. Symptoms include:

• Wheezing, difficulty breathing
• Swelling of the tongue
• Hypotension (low blood pressure)
• Shock
• Hives
• Abdominal cramping
• Fainting, faintness

Always call 911 in the event of suspected anaphylaxis. It’s important to note that if you have experienced anaphylaxis in the past, you have a 25-65% chance of experiencing it again if you’re stung.

When to go in, when to call a doctor

Call 911 immediately if someone stung by a bee has any of the symptoms mentioned above or has had a life-threatening reaction to a sting in the past.

Visit the emergency department or urgent care if you experience any of the following within two hours of being stung:

• Hives, itching or swelling somewhere on your body other than where you were stung
• Vomiting or abdominal cramps
• You have a history of anaphylaxis and you used ephedrine shot (also known as an EpiPen), and you’re experiencing no symptoms (this is to confirm no need of oral steroids)

Visit urgent care or primary care if you’re experiencing:

• A sting inside your mouth
• A sting on your eyeball
• More than 50 stings
• Fever and area of the sting is red or tender
• A red streak on your skin greater than two inches

Call your doctor or the nurse helpline if:

• It’s been 24 hours and the site has become red and very tender
• It’s been 48 hours and the site is increasing in size
• Swelling has increased over four inches and has spread over your wrists or ankle
• Hives have developed after three days
• Your sting has become infected, and it has not improved after three days

Get care for a bee sting

The best bee sting treatments and remedies are probably right in your own home. From ointments to cold packs, everything you need to treat these pesky stings is likely in your cupboard. But we’re here if you have any questions or need advice. You can call our nurse line or make an appointment with one of our primary care doctors.

Now that you know what to look for, keep an eye out for warning signs of an allergic reaction to bee stings. Knowing what to look for and how to treat bee stings could just save a life.

Like many other conditions, gum disease can be sneaky. In its earliest stages, you may not notice anything has changed with your teeth or gums – especially if it’s been a while since your last dental checkup.

So, what exactly is gum disease and what symptoms might you be able to spot? Keep reading to get the answers to these questions and more.

What is gum disease?

Gum disease, also called periodontal disease, is an infection of the gums and other tissues surrounding the teeth.

What causes gum disease?

Gum disease can occur when too much plaque builds up on teeth. Our mouths are always forming plaque, which contains bacteria that feed on the sugar and starches in the things we eat and drink. Without good oral hygiene habits, diet and regular dental checkups, plaque builds up and hardens, which is called tartar or calculus.

Once tartar has formed, it acts as a “home” for bacteria. This allows bacteria to grow and continuously expose your teeth and any surrounding tissue to acid, which can lead to inflammation. This can also cause mechanical irritation to your gums, which can lead to ulcers. Inflammation can eventually start to break down the affected tissues and bone, giving bacteria more room to grow, and damaging your teeth and gums.

What are the stages of gum disease?

There are two different stages of gum disease: gingivitis and periodontitis.

Gingivitis

Gingivitis is the earliest stage of gum disease, where symptoms are usually mild and limited to the tissues surrounding the teeth. If gum disease is caught and treated at this stage, it usually can be treated without major damage to your gums. But if left untreated, it can progress into periodontitis.

Periodontitis

Periodontitis is more severe gum disease where infection has spread below the gums, damaging the tissues and bone that support the teeth. There are three stages of periodontitis disease: early periodontitis, moderate periodontitis and advanced periodontitis. There are specific markers for each stage, which are used by dentists during diagnosis.

Gum disease symptoms

The early stages of gum disease often don’t involve any pain or discomfort. This makes it important to look out for other signs like visual changes to your gums or teeth. The longer gum disease is left untreated, the more damage it can cause and the more costly it can be to treat. So if you notice one or more of the symptoms below, it’s best to see a dentist as soon as possible.

What does gum disease look like?

Healthy gums are light pink, firm and fit tightly around teeth, while infected gums can be:

• Swollen or puffy
• Dull red (more common with gingivitis)
• Bright red or purplish (more common with periodontitis)

Other early signs of gum disease

The most common signs of early gum disease are:

• Gums that bleed easily when you brush or floss
• DBad breath
• Gums that pull away from the teeth
• Tender gums (sometimes)

Signs of more advanced gum disease

In addition to the early signs above, symptoms of more advanced gum disease include:

• A pink tinge to your toothbrush after brushing
• Spitting out blood when brushing or flossing your teeth
• Bad breath that won’t go away
• Painful chewing
• New spaces developing between your teeth
• Pus between your teeth and gums
• Loose teeth or loss of teeth
• Changes in how your teeth fit together when you bite

   
 

How is gum disease diagnosed?

To diagnose gum disease, a dentist will examine your mouth for symptoms like tartar buildup, easy bleeding and receding gums. They’ll also review your dental and medical histories for possible risk factors.

A dentist may also use a dental probe as part of the diagnosis, and to determine what stage of gum disease you have. This is done by measuring the depth of the spaces (or pockets) between your teeth and your gums, and checking for any loss of the connective tissue that holds your teeth in their sockets. X-rays may also be taken to check for bone loss around them.

• A healthy mouth generally has pockets that are 1-3 millimeters deep.
• Mild periodontitis is defined as two or more pockets with at least 3 millimeters of connective tissue loss, and two or more pockets that are at least 4 millimeters deep, or one pocket that’s 5 millimeters deep.
• Moderate periodontitis is defined as two or more pockets with at least 4 millimeters of connective tissue loss, or two or more pockets that are at least 5 millimeters deep.
• Severe periodontitis is defined as two or more pockets with at least 6 millimeters of connective tissue loss, and one or more pockets that are at least 5 millimeters deep.

How do you prevent gum disease?

Good oral hygiene is key to preventing gum disease. For your daily life, this means brushing at least twice a day and flossing between your teeth once a day. But good oral hygiene also means following a dentist-recommended schedule of regular dental checkups. These checkups are opportunities to get your teeth cleaned more deeply than you can clean them at home, and they also allow your dentist to catch and treat signs of oral health issues like gum disease before they become severe.

In addition, there are lifestyle factors that can help keep your mouth healthy. Two of the biggest are:

• Eating a balanced diet. Proper nutrition keeps your immune system strong, which makes it more effective at fighting infections like gum disease. It’s also important to limit excess sugar since it’s what the bacteria that cause gum disease feed on.
• Not using tobacco products. Tobacco use (as well as smoking of any kind) increases your risk of gum disease and makes it harder for your body to fight infections.

Other gum disease risk factors

• Age
• Stress
• Obesity
• Family history of gum disease
• Uncontrolled diabetes
• A suppressed immune system from medication or health conditions
• Changes in hormone levels, such as during pregnancy or while using hormonal birth control
• Conditions that affect inflammation, such as rheumatoid arthritis or Crohn’s disease

How do you treat gum disease?

Gum disease that’s progressed beyond gingivitis requires professional treatment, but successful treatment depends on you, too.

To make sure gum disease doesn’t come back in the future, it’s important to address any risk factors you have, in the same way that you would if you were trying to prevent it in the first place. This could include improving your oral hygiene, changing your diet, losing weight, quitting smoking or managing chronic health conditions like diabetes.

Professional treatment for less advanced cases of gum disease typically involves root planing and scaling (deep cleaning). Planing and scaling may take multiple visits to complete. At HealthPartners Dental, we provide a local anesthesia or anesthetic rinses to help keep our patients comfortable during deep cleanings.

• Scaling is the process of removing plaque and tartar from your teeth.
• Root planing is smoothing the surface of a tooth’s root. This makes it harder for bacteria to build up and makes it easier for the gums to reattach if inflammation caused them to separate from the teeth.
• Antibiotics help get rid of the infection-causing bacteria. Antibiotics may come in the form of pills, rinses or gel inserts placed in infected pockets after scaling and planing.
  • Gum surgery may be necessary for advanced cases of gum disease.

Look after your oral health

If you’re noticing pain in your mouth, bleeding gums or other unusual symptoms, don’t ignore them. Without treatment, gum disease may advance and lead to more painful and costly dental problems. A dentist can examine your mouth for issues, provide the exact treatment you need and offer expert recommendations that will help keep your teeth strong and healthy for years to come.

   
 

Red, swollen or tender gums. Bad breath that doesn’t go away. Bleeding when you brush or floss. While any of these mild symptoms could be ignored, if you’re noticing them regularly it’s time to pay attention.

That’s because they could be early symptoms of gum disease , which is called gingivitis. If left untreated, gingivitis can lead to more serious gum disease and dental issues. But the good news is that gingivitis is completely reversible if it’s caught and treated early.

What causes gingivitis?

Gingivitis is most commonly caused by insufficient oral hygiene such as not brushing enough, not flossing enough or not having regular dental checkups. Without good oral hygiene, plaque builds up on your teeth, and can harden into tartar. Plaque and tartar contain bacteria, and these bacteria can damage your gingiva, leading to inflammation.

What are gingivitis symptoms?

Symptoms of gingivitis can include one or more of the following:

• Swollen or puffy gums
• Gums that are dusky red rather than pale pink
• Gums that bleed easily when you brush or floss
• Gums that pull away from the teeth (receding gums)
• Tender gums
• Bad breath

When should you see a dentist for gingivitis symptoms?

Having one or more of the above symptoms is reason to see a dentist. But in general, any amount of pain or bleeding in your mouth means it’s time to make an appointment. It can be easy to ignore a little irritation, but it’s important to treat oral health conditions like gingivitis as early as possible.

   
 

How is gingivitis diagnosed?

To diagnose gingivitis, a dentist will closely examine your teeth and gums for signs of inflammation, recession and more. They may also ask you questions about your medical and dental histories to find out if you have any risk factors for gingivitis, such as tobacco use or a family history of gum disease.

The dentist or dental hygienist may also measure the depth of the spaces or “pockets” between your teeth and the gum tissue surrounding them. Pockets in a healthy mouth are generally 1-3 millimeters deep. X-rays may also be taken to check for any bone loss.

Is gingivitis curable?

Generally, yes. If gingivitis is caught early, before any permanent damage has occurred, your gums can recover.

Can you get rid of gingivitis on your own?

Taking steps to improve your oral hygiene can certainly help reduce gingivitis symptoms. But a dental exam is needed to determine how advanced gum disease is. For example, plaque can be removed with good brushing and flossing, but tarter buildup needs to be removed by a dental hygienist.

How do you prevent gingivitis?

There are several oral hygiene habits and lifestyle changes you can make to prevent gingivitis from developing or coming back, including:

• Brush your teeth at least twice a day, using a soft toothbrush or an electric toothbrush.
• Floss at least once a day. If you have difficulty flossing, your dentist and dental hygienist can provide you with helpful tools to make this easier.
• Eat a healthy diet to support your immune system and cut down on between-meal snacking. Snacks typically contain sugar which the bacteria in plaque feed on.
• Consider quitting smoking or vaping. Tobacco use contributes to plaque buildup and slows down the healing process. Your dentist and dental hygienist can offer support and resources to help.

How is gingivitis treated?

In addition to the steps you take on your own, a dentist may treat gingivitis with:

• Scaling and root planing– Some people call this a deep cleaning. Scaling is the process of using a specialized tool to remove tartar and plaque from your teeth. Root planing is removing bacteria from and smoothing the surface of the root tissue on a tooth below the gum line. Smooth root surfaces heal better and make it harder for bacteria to grow.
• Dental restoration (fillings)– If there are structural issues in your mouth that make oral care harder or that are contributing to irritation, a dentist may suggest fixing them. Common examples include poorly fitting crowns or fillings.
• Oral care recommendations– These may include prescriptions for specific toothpastes or mouthwashes, tips for improving your daily oral hygiene and a suggested schedule for dental checkups.

What happens if you don’t treat gingivitis?

If left untreated, gingivitis can develop into more advanced gum disease, which is known as periodontitis. Symptoms of periodontitis are more severe, and it can lead to serious infection, bone loss and tooth loss.

Don’t wait to look after your oral health

Oral health issues are best treated early, before they become more painful and expensive. So if you’re noticing changes in your mouth that could be signs of gingivitis, or if you have any other concerns about your oral health, making an appointment with a dentist is your next step.

At your appointment, you’ll receive a dental exam, and your dentist will work with you to address any oral health concerns you have.

   
 

Jacob Bor has been thinking about a parallel universe. He envisions a world in which America has health on par with that of other wealthy nations, and is not an embarrassing outlier that, despite spending more on health care than any other country, has shorter life spans, higher rates of chronic disease and maternal mortality, and fewer doctors per capita than its peers. Bor, an epidemiologist at Boston University School of Public Health, imagines the people who are still alive in that other world but who died in ours. He calls such people “missing Americans.” And he calculates that in 2021 alone, there were 1.1 million of them.

Bor and his colleagues arrived at that number by using data from an international mortality database and the CDC. For every year from 1933 to 2021, they compared America’s mortality rates with the average of Canada, Japan, and 16 Western European nations (adjusting for age and population). They showed that from the 1980s onward, the U.S. started falling behind its peers. By 2019, the number of missing Americans had grown to 626,000. After COVID arrived, that statistic ballooned even further—to 992,000 in 2020, and to 1.1 million in 2021. Were the U.S. “just average compared to other wealthy countries, not even the best performer, fully a third of all deaths last year would have been prevented,” Bor told me. That includes half of all deaths among working-age adults. “Think of two people you might know under 65 who died last year: One of them might still be alive,” he said. “It raises the hairs on the back of my neck.”

These counterfactuals puncture two common myths about America’s pandemic experience: that the U.S. was just one unremarkable victim of a crisis that spared no nation and that COVID disrupted a status quo that was strong and worth restoring wholesale. In fact, as one expert predicted in March 2020, the U.S. had the worst outbreak in the industrialized world—not just because of what the Trump and Biden administrations did, but also because of the country’s rotten rootstock. COVID simply did more of what life in America has excelled at for decades: killing Americans in unusually large numbers, and at unusually young ages. “I don’t think people in the United States actually have any awareness of just how poorly we do as a country at letting people live to old age,” Elizabeth Wrigley-Field, a sociologist at the University of Minnesota, told me.

---

Although Bor’s study has yet to be formally reviewed, Wrigley-Field and five other independent researchers vouched for its quality to me. “The paper is extremely important, and the researchers who produced this know what they’re doing,” Steven Woolf, a population-health expert at Virginia Commonwealth University, told me. “It builds on, and considerably expands, what we’ve already known.”

Several studies, for example, have shown that America’s life expectancy has tailed behind other comparable countries since the 1970s. By 2010, that gap was already 1.9 years. By the end of 2021, it had grown to 5.3. And although many countries took a longevity hit because of COVID, America was once again exceptional: Among its peers, it experienced the largest life-expectancy decline in 2020 and, unlike its peers, continued declining in 2021. But Bor says that people often misinterpret life-expectancy declines, as if they simply represent a few years shaved off the end of a life. Someone might reasonably ask: What’s the big deal if I die at 76 versus 78? But in fact, life expectancy is falling behind other wealthy nations in large part because a lot of Americans are dying very young—in their 40s and 50s, rather than their 70s and 80s. The country is experiencing what Bor and his colleagues call “a crisis of early death”—a long-simmering tragedy that COVID took to a furious boil.

In every country, the coronavirus wrought greater damage upon the bodies of the elderly than the young. But this well-known trend hides a less obvious one: During the pandemic, half of the U.S.’s excess deaths—the missing Americans—were under 65 years old. Even though working-age Americans were less likely to die of COVID than older Americans, they fared considerably worse than similarly aged people in other countries. From 2019 to 2021, the number of working-age Americans who died increased by 233,000—and nine in 10 of those deaths wouldn’t have happened if the U.S. had mortality rates on par with its peers. “This is a damning finding,” Oni Blackstock, the founder and executive director of Health Justice, told me.

Read: How did this many deaths become normal?

The crisis of early death was evident well before COVID. As many studies and reports have shown, since the turn of the 21st century, “midlife ages are where health and survival in the U.S. really go off the rails,” Wrigley-Field told me. “The U.S. actually does well at keeping people alive once they’re really old,” she said, but it struggles to get its citizens to that point. They might die because of gun violence, car accidents, or heart disease and other metabolic disorders, or drug overdoses, suicides, and other deaths of despair. In all of these, the U.S. does worse than most equivalent countries, both by failing to address these problems directly and by leaving people more vulnerable to them to begin with.

Consider how many years the missing Americans would have collectively enjoyed had they survived—all the birthdays and anniversaries that never happened. In other rich countries, the total “years of life lost” have flatlined for the past five decades. In the U.S., they have soared: In 2021 alone, the 1.1 million missing Americans lost 25 million years of life among them. That number doesn’t account for the events that preceded many of these deaths—the “years of disability, illness, and loss of human potential, creativity, and dignity,” Laudan Aron, a health-policy researcher at the Urban Institute, told me. And, especially in the case of middle-aged deaths, they left behind young dependents, whose own health might suffer as a result. The sheer number of missing Americans, and the “profound ripple effects” of their absence, are “really hard to wrap one’s head around,” Aron said.

Read: The final pandemic betrayal

These staggering numbers also help contextualize COVID’s toll. The coronavirus caused the largest single-year rise in mortality since World War II, becoming the third leading cause of death in the U.S., after only heart disease and cancer. But this enormous tragedy unfolded against an already tragic backdrop: The number of missing Americans from 2019 is larger than the number of people who were killed by COVID in 2020 or 2021. This isn’t to minimize COVID’s impact; it simply shows that in the Before Times, America had “very successfully normalized to an extremely high level of death on the scale of what we experienced in the pandemic,” Justin Feldman, a social epidemiologist at Harvard, told me. And when COVID drove those levels skyward, America proved that “we’ll accept even more deaths compared to our already poor historical norms,” Feldman said.

Such deaths, though obvious on a graph, are hidden from Americans with social privilege. In the summer of 2020, Bor remembers having an outdoor barbecue with a friend who grew up in a low-income housing project. “At that point, six months in, he knew six people in his close circle who had been killed by COVID,” Bor told me. “I still don’t.” The fact that half of the working-age Americans who died last year should still be alive “isn’t visceral if you haven’t lost anyone,” he said.

---

The current mortality crisis was long in the making. In terms of mortality, America’s peer countries—many of which had been hammered by World War II and its aftermath—began catching up with it in the mid-1970s before overtaking in the early 1980s. That was a pivotal era, when globalization, automation, and a growing service industry led to huge losses in mining, manufacturing, and other blue-collar sectors. The U.S. profoundly failed to protect its citizens from these changes. Its social safety net—state assistance for parents, or people facing job, food, or housing insecurity—was meager; its public-health system was languishing after decades of underinvestment; and unlike every other wealthy country, it lacked universal health care. These factors “privatized risk,” Bor and his colleagues wrote in their paper, “tying health more closely to personal wealth and employment.” As labor unions declined and minimum wages stagnated, more Americans had fewer resources to lean on if their health declined. Poorer Americans already lived, on average, shorter lives than rich ones, and that gulf started to widen.

Other particularly American choices exacerbated the stresses on the health of the country’s citizens, again weighing more heavily on less wealthy people. A growing mass-incarceration industry punished them. A deregulatory agenda that began with Ronald Reagan’s administration left them vulnerable to unhealthy foods, workplace hazards, environmental pollutants, guns, and opioids. “America basically says: If you’re poor, you don’t have access to safe choices,” Bor told me.

Factors like social inequalities and frayed social safety nets are the fundamental weaknesses of American society, which more specific problems like opioids, metabolic disorders, and COVID exploit. During the pandemic, for example, poor and minority groups were more likely to be infected because they lived in crowded housing, distrusted medical leaders, and couldn’t work from home or take time off when sick. And instead of addressing these foundational problems, policy makers instead focused on personal responsibility.

America’s drastic underperformance in health also stems from its history of segregation and discrimination. Racist policies have obviously harmed the health of minorities. But as the policy expert Heather McGhee and the physician Jonathan Metzl have independently argued, elites have long marshaled the racial resentment of poor white Americans to undermine support for public goods that would benefit everyone, such as universal health care. Per Frederick Douglass and other Black leaders, “They divided both to conquer each.”

Read: How public health took part in its own downfall

COVID, for example, disproportionately killed Black, Latino, and Indigenous Americans—a trend that, when highlighted to white people, reduces their concern about the pandemic and their support for safety measures. But in 2021, young white Americans still died at three times the rate of the average resident of other peer nations, while young Black and Indigenous Americans died at rates five- and eightfold higher, respectively. “There are thousands of racial-disparity studies that compare Black people to white people—but white Americans are a terrible counterfactual,” Bor told me. They’re frogs in the same pot, boiling more slowly but boiling nonetheless. By using them as a baseline, we ignore how “everyone is harmed by the status quo in the U.S.,” Blackstock told me, while also underestimating how dire things really are for people of color. (The same problem applies to income inequality: White Americans living in the richest 1 percent of counties still have higher rates of maternal and infant mortality than the average residents of wealthy countries.)

So, “what happens now?” Bor asked me. “Are we going to have 1 million missing Americans a year, every year, going forward? Or more?” His study doesn’t suggest a reason for optimism, but it does provide a defense against nihilism. The entire concept of missing Americans is rooted in a comparison with other countries, which shows that these early deaths aren’t inevitable. The U.S. could at least start moving in the direction of its peers by adopting policies that work elsewhere, such as universal health care, minimum-wage increases, federally required paid sick leave, and better unemployment insurance.

But “the inability of our politics to generate policies that manage health threats is grim,” Bor said. None of the weaknesses that COVID exposed have been addressed; some, like the chasm-sized health gaps between rich and poor or white and Black, have been widened. Vaccines significantly reduce the risk of dying from COVID, but their power is blunted by low uptake, new variants, the lifting of almost all infection-thwarting protections, and the looming loss of COVID funding. Reactionary laws that hamstring what public-health departments can do in emergencies will make the U.S. vulnerable to the new viruses that will inevitably assault it in future years. America’s already underperforming health-care system has been badly battered by the pandemic, and weakened by waves of health-care-worker resignations. In recent months, the Supreme Court has constrained both gun and carbon-emission regulations, while clearing the road for states to restrict or ban abortions—a move that could easily boost America’s already sky-high maternal mortality rates. The climate is still changing rapidly, exposing people who have no choice but to work outside to the ravages of heat.

As much of the country returns to normal, Bor’s study makes plain what normal actually meant—and, as I wrote in 2020, that normal led to this. “A lot of Americans may be under the impression that we had a bad go of it during COVID, and once the pandemic is over, they can go back to having the best health in the world,” Woolf told me. “That is a gross misconception.”

In early July, Sebastian Kohn, a 39-year-old nonprofit professional in Brooklyn, woke up with a fever, a sore back, and swelling in the lymph nodes of his throat and groin. He took a COVID test, which was negative. But Kohn had some clue as to what might be going on. Pride celebrations had taken place a week earlier, and a newly infamous disease was circulating largely in the gay community: monkeypox.

Suspicious that he might have the viral illness, Kohn immediately isolated. Two days later, a painful, itchy rash appeared in an intimate location. He knew then that he was in for a ride. Kohn found an urgent-care center where a doctor was able to swab his skin lesions and send them off to a lab, where technicians searched for signs of the virus’s genetic material. Then he waited, alone, in his home.

More than 15,000 monkeypox cases have been confirmed around the world since the outbreak began in May, but the condition, which spreads through close contact with the rash or body fluids of an infected individual, has been difficult to diagnose because of a lack of available testing. New York City was at one point able to test only 10 patients a day. When Kohn got sick, the system was still running at significant delays. While an analogous COVID test can be turned around by the next day in many cases, Kohn’s positive result for monkeypox took four days to arrive—all while a blistering rash spread out across his body. (Six days after that, Kohn received a phone call from a contact tracer working for the local department of health. He may have been exposed to monkeypox, the person warned.)

Read: Gay men need a specific warning about monkeypox

In terms of sheer numbers, the nation’s monkeypox-testing capacity has increased dramatically since Kohn’s run-in with the system. On Monday, the Centers for Disease Control and Prevention announced that the U.S. is now capable of evaluating 80,000 cases a week, up from 6,000 initially. But another, more important bottleneck remains stubbornly in place: The CDC’s official guidance recommends that labs test for monkeypox using only samples of a patient’s skin, taken at the site of a visible rash. As a result, people like Kohn, whose fever and swollen lymph nodes come on a few days before their lesions, must let the illness grow before it can be diagnosed. Others may develop hidden sores in their mouth or anus, and not realize that they can be tested. And many more without symptoms will be left to wait and wonder, after an exposure, whether they might have been infected.

As the outbreak spreads—with more than 2,000 cases in the U.S., by the latest count—public-health authorities have doubled down on this restriction: Testing for the virus must make use of swabs taken from a lesion, according to a “Safety Communication” issued by the Food and Drug Administration last Friday. “The FDA is not aware of clinical data supporting the use of other sample types, such as blood or saliva, for monkeypox virus testing,” the communication said, and testing of these other types “may lead to false test results.” This alarming messaging, delivered at a crucial moment in the virus’s spread, will have a profound effect on how quickly new monkeypox infections can be identified, isolated, and treated.

With this disease, like many others, early detection is invaluable as a means of promoting early treatment. Vaccination shortly after exposure can prevent monkeypox from occurring in many cases, and inoculation during the early phase of illness may reduce the severity of symptoms or curtail the contagious period. Although no medications have been approved specifically for monkeypox, several antivirals originally meant for smallpox are thought to help. As we have seen with the COVID antivirals Paxlovid and remdesivir, these types of therapies tend to work best when given as early as possible.

It may be just as important to identify those infected asymptomatically. An intriguing study out of Belgium, posted earlier this month but not yet peer-reviewed, examined swabs taken from the mouth and anus of 224 men in May. Samples had originally been collected to look for gonorrhea and chlamydia, but the scientists found monkeypox DNA in three of them. None of those men reported any symptoms of disease before or after testing, nor did any of their close contacts. Nevertheless, the study’s authors believe that these and other potential asymptomatic carriers could well be contagious. (Guidance from the CDC, last updated at the end of June, says that spreading can happen only after symptoms start.) In the meantime, other studies, conducted in Europe and Africa, have shown that monkeypox DNA is in many cases detectable in saliva, blood, urine, and rectal samples, even before a rash appears.

Read: The U.S. is underreacting to monkeypox

Matt Ford, a 30-year-old actor and video producer who lives in Los Angeles and New York, told me that he suspects he passed the virus on during the very early phase of his infection. He caught monkeypox last month, and was subsequently placed under public-health isolation. But in the week between his exposure and when he first noticed skin spots, he said, he spent an evening with a guy he was seeing. That guy would later come down with the disease himself. In retrospect, Ford had been a little tired during that time, but he had not felt unwell enough to pay it any mind. If people really are passing on the virus with few to no symptoms—and we don’t know for sure—then an early-detection test collected by mouth, vein, or rectal swab might prevent this onward spread.

Yet last week’s warning from the FDA was very specific: Unless you have an active rash, don’t bother to get tested. When I asked the agency what specific data it was relying on for its safety communication, an FDA spokesperson repeated only that the organization is “not aware of clinical data supporting asymptomatic testing or testing samples other than those taken directly from a suspect lesion.” CDC Director Rochelle Walensky also confirmed to reporters last week that a skin lesion is required for testing from her organization’s perspective, though she said that the CDC is exploring the possibility of saliva, throat, and blood tests.

This “absence of evidence” maneuver by authorities should be quite familiar at this point. In December 2019 and January 2020, the Chinese government publicly stated that there was no clear evidence of human-to-human transmission of the new coronavirus, and the World Health Organization repeated the claim. Three months later, in April, officials from the WHO cited “no evidence” that wearing masks prevented COVID transmission in a wider community setting. In the case of monkeypox testing, such conservatism is particularly self-defeating. When public-health authorities warn of a lack of clinical data for the effectiveness of blood and saliva tests, they are not only ignoring a small but growing list of published studies; they are also making it that much harder for researchers to collect more clinical data. The FDA and the CDC should be encouraging labs to run and evaluate new tests, Jay Varma, a public-health physician and professor at Cornell, told me. Instead the agencies are telling labs to stay away from them.

The FDA is correct that any new test for monkeypox would almost certainly produce some false results. (Even the gold-standard skin tests for monkeypox can misclassify cases.) But the advantages of having an early diagnostic for monkeypox are beyond dispute: Most people would take precautions to reduce their chance of exposing others if they knew they were infected, and contact tracers could hunt down additional cases far more quickly.

Ideally, one could imagine integrating monkeypox testing into the sexual-health infrastructure that is already in place. Many members of the gay community are used to receiving regular screening for HIV and other sexually transmitted diseases, according to Joseph Osmundson, a clinical assistant professor of biology at NYU. “There is a real desire in the community for scale testing” for monkeypox, too, he told me. Throat and rectal swabs collected for gonorrhea and chlamydia, for example, could also be tested for the virus. Varma suggests checking participants at any event where casual sex is expected to occur.

As things stand, physicians, patients, and laboratories would have to defy the explicit advice of U.S. public-health authorities in order to make this happen. Labs are legally permitted to create their own monkeypox diagnostics, even in the face of the FDA’s official warnings. Indeed, some organizations have already begun doing so. (If the U.S. government were to formally declare monkeypox a public-health emergency—as some politicians are calling for—then, ironically, this regulatory flexibility could be revoked.) Benjamin Pinsky, the medical director of the clinical-virology lab at Stanford, has overseen the testing of more than 70 patients for monkeypox, using samples from the nose, mouth, rectum, and bladder, as well as traditional skin scrapings. The newer methods have already picked up a few cases, he told me, but developing those tests without the cooperation of the government has been difficult. Pinsky said that public-health labs initially refused to provide him with real patient samples to confirm the validity of his approach. Many less-experienced lab directors will be dissuaded entirely from setting up their own protocols, because designing a diagnostic from scratch is far more complicated than using an off-the-shelf tool provided by the government. Also, no lab director would be eager to explain to hospital administrators why he or she is openly flouting an official safety warning.

One need only look back at the COVID testing snafus of 2020 to get a sense of what can happen when the government works against, rather than with, the medical community. At the start of the pandemic, the FDA prohibited labs from developing their own COVID-detection methods without first completing an arduous authorization process. Hospitals were encouraged to rely on the CDC’s official test, just as they are now for monkeypox. The government COVID test turned out to have a serious manufacturing defect, which thankfully hasn’t been repeated during the monkeypox outbreak. But excess caution remains a problem, and has once again left the country dangerously short of diagnostic capacity. U.S. hesitation also puts the country out of step with the international community. The WHO, parts of Canada, and the United Kingdom, for instance, all recommend analyzing a throat swab in some circumstances.

It’s not that the FDA’s concerns are unfounded. A monkeypox-testing bonanza, in which anyone and everyone can start to market their own services with limited oversight, could have undesirable consequences. Once the rules were loosened for COVID tests, small and inexperienced laboratory outfits served up diagnostic errors on occasion, or engaged in exploitative practices. But most labs follow proper quality-control procedures, and the Centers for Medicare and Medicaid Services still provides routine supervision. Any risk of false results in such an environment must be weighed against the more serious consequence of missing cases entirely. Less testing for monkeypox this summer will inevitably lead to more people suffering from ulcerating rashes, drenching night sweats, malodorous rectal discharge, and expansive onward spread.

Members of the gay community want easier and earlier testing for monkeypox. Public-health experts want the same thing. Aggressive case-finding may be the only way to get the current outbreak under control, and most large labs have the ability to detect the presence of monkeypox DNA in a variety of body fluids. We don’t yet know the real-world performance of a monkeypox-screening program based on all these fluids, but doctors could and should be coordinating with one another and with public-health agencies to find out. “We want the best diagnostics, the best vaccines, the best treatment protocols, and the best science in the world,” Osmundson told me. “But we are also in an emergency, and people are getting sick, and they are not able to access the care they need.”

And there it is: President Joe Biden has tested positive for the coronavirus, the White House announced Thursday morning, and is dosing up with Paxlovid to keep his so-far “very mild symptoms” from turning severe.

In some ways, this is one of the cases the entire world has been waiting for—not sadistically, necessarily, but simply because, like so many other infections as of late, it has felt inevitable. Once, it might have seemed possible to avoid this virus; now most Americans have had it. SARS-CoV-2 has been spewing out variants and subvariants at an absolutely blistering clip, and wave after wave of infections has slammed the nation, collapsing case peaks into a never-ending plateau. Vice President Kamala Harris caught the coronavirus in April; Anthony Fauci got it in June.

Perhaps the most notable aspect of these high-profile cases is not that they happened, but when. Though certainly on the front lines of the country’s COVID response, these officials have enjoyed the privilege of protection throughout the pandemic, with access to masks, tests, vaccines, and, most recently, antivirals; the comfort and security of jobs that can be done while in isolation; the socioeconomic means to separate themselves from colleagues and loved ones, and the support staff to alert close contacts about exposures. They, as much as anyone feasibly could, “have had access to all the available tools” the country has to fight the coronavirus, says Anne Sosin, a public-health researcher at Dartmouth College, so much so that they’ve even had the liberty to get a bit avant-garde. Fauci, for instance, received two courses of Paxlovid when his symptoms vanished and then reappeared—an unsanctioned use of the drug that sparked some criticism from infectious-disease experts who thought the move unwarranted and potentially baffling for a public unsure of who should be taking the drug and how.

Avoiding the virus, or at least a known, test-confirmed infection, up until this point of the pandemic does have real value. In the U.S., our collective capability to evade any serious outcome is much higher than it was in, say, October 2020, when then-President Donald Trump tested positive. Trump’s tussle with the virus unfurled at a time before COVID vaccines were available, and his doctors treated his illness as a pressing medical emergency, rushing him to the hospital for observation and treatment. At the time, COVID therapies were focused on the severely sick, and had to be administered by a trained health-care professional, typically in a medical setting; like Biden, Trump got the best care that was available at the time, but in the first year of the crisis, that entailed the trifecta of remdesivir, steroids, and still-experimental monoclonal antibodies, which Trump later touted, misleadingly, as a “cure.” Most monoclonal-antibody treatments, including the specific cocktail Trump received, have since fallen out of use because they’re less effective against the variants circulating today.

Today, President Biden may not need anything beyond Paxlovid, which the FDA greenlit late last year and can be taken as a pill at home. “We know so much more now,” says Taison Bell, a critical-care and infectious-disease physician at UVA Health. “We understand what treatments work, what treatments don’t.” Although Biden is 79—an age that puts him at high risk of severe outcomes from the virus—he’s quadruply vaccinated, having received his second booster in late March. And clinical trials have shown Paxlovid to be nearly 90 percent effective at slashing the risk of COVID hospitalizations or deaths (though those data were gleaned from an entirely unvaccinated population; real-world estimates of the drug’s performance have been far more mixed). Kevin O’Connor, the president’s physician, wrote in a letter today that “I anticipate that he will respond favorably, as most maximally protected patients do.”

In the third year of the pandemic, just as unsurprising as Biden’s illness is the pressure for the White House to leverage it as a statement on the right approach to COVID control. In 2020, Trump alarmed experts by peeling off his mask and walking into the White House just after being discharged from the hospital that treated him for COVID. Nearly two years later, Biden, to begin with, is apparently modeling some version of business as usual: The White House has already announced that he “continues to carry out the full duties of the office while in isolation” … which somehow involves the country’s chief decision maker tweeting out maskless photos (taken by someone else, presumably) of himself doing paperwork at his desk.

But, like Trump’s, Biden’s experience—including any performative professional displays—is still an exception among exceptions. “The president, as we would want, has access to therapies,” says Utibe Essien, a physician and health-equity researcher at the University of Pittsburgh. “We would hope that everyone should.”

They do not. Although the White House has made plenty of noise about the need for funding to keep the country awash in tests, treatments, and vaccines, Congress has not provided those resources, and the administration has not marshaled the political will to change that situation. Nor has it sparked the enthusiasm necessary to reignite America’s pandemic response where it has flagged. Cases remain undercounted; tests remain underused. Vaccination rates—especially boosting rates—remain worrisomely low. Effective treatments have been collecting dust on shelves amid enormous disparities in access. And gathering restrictions and masks are now mostly mitigation measures of the past, even though the CDC’s loosened guidelines currently recommend that people in more than a third of the country’s counties should be covering their face to control the coronavirus’s spread. At the beginning of this month, in a Fourth of July celebration, the president crowed that the country was “closer than ever to declaring our independence from a deadly virus”; weeks later, he is playing host to that same foe. And although he might have had access to the tools needed to combat it, “that doesn’t mean they’re going into the hands of the people who need them,” Essien told me.

That the president’s infection happened now, during the nation’s roiling, months-long, multi-subvariant wave, speaks to the bad cycle that the country has found itself in. The current surge shows few signs of slowing; more iterations of the virus are undoubtedly on their way. And yet little is being done in response to the danger, let alone as a preventive to keep the situation from going further off the rails. The U.S. has defaulted to acceptance, Sosin told me, of the status quo: uncontrolled transmission, viral evolution on loop.

Biden could have delayed his encounter with the disease a bit longer, buying time for the development of even better antivirals, clarity on the risks of long COVID, or, at the very least, fall’s highly anticipated BA.4/5 vaccine update. Doing that, though, would have required more investment—from him, perhaps, as an individual, but in particular from his country, under his leadership, to collectively tamp down transmission. In this current environment, however, “the virus has that many more pathways to spread through the community,” Bell told me—up to and including the president.

I am on a mission to preserve the most valuable item in my home: my fiancé, who has never had COVID. Through sheer luck and a healthy dose of terror, he made it through the first pandemic year without getting sick. Shielded by the J&J vaccine and a Moderna booster, he dodged infection when I fell ill last November and coughed up the coronavirus all over our cramped New York City apartment. Somehow, he ducked the Omicron wave over the winter, when it seemed as though everyone was getting sick. And in the past few months, he has emerged unscathed from crowded weddings, indoor dinners, and flights across the country.

At this point, I worry about how much longer it’s going to last. People like him—I think of them as “COVID virgins”—are becoming a rare breed. Just yesterday, President Joe Biden thinned their ranks by one more person. The Institute of Health Metrics and Evaluation suggests that as of earlier this month, 82 percent of Americans have been infected with the coronavirus at least once. Some of those people might still think they’re never had the virus: Asymptomatic infections happen, and mild symptoms are sometimes brushed off as allergies or a cold. Now that we’re battling BA.5, the most contagious and vaccine-dodging Omicron offshoot yet, many people are facing their second, third, or even fourth infections. That reality can make it feel like the stragglers who have evaded infection for two and a half years are destined to fall sick sooner rather than later. At this point, are COVID virgins nothing more than sitting ducks?

Read: Of course Biden has COVID

The basic math admittedly doesn’t look promising. Most of the people getting infected right now seem to be coming down with the illness for the first time, even though they are a distinct minority. Nationally, we don’t have good data on who is getting COVID, though in New York, first infections seem to be  happening at five times the rate of reinfections. Part of why those who haven’t gotten COVID seem to be at a higher risk of infection is that taking into account all other factors—vaccination, age, behaviors—they lack the immunity bump conferred by a bout with the virus, no matter how fleeting that bump may be. On its own, this would suggest that these people are in fact sitting ducks who can’t avoid infection short of hunkering down in total isolation.

The experts I talked with agreed that the risk of infection is currently high. “We are finding now that with the more transmissible variants, it’s becoming more and more difficult to avoid infections,” Robert Kim-Farley, an epidemiologist at UCLA, told me. “However, it’s not inevitable.” Rick Bright, the CEO of the Rockefeller Foundation’s Pandemic Prevention Institute, was less certain. “Honestly, it might be inevitable, the way the virus has continued to change,” he said.

Still, they reiterated that we still don’t quite know just how at risk those who haven’t had COVID are—especially when BA.5 seems to be reinfecting so many people. “I don’t know if I would call them sitting ducks, necessarily,” Bright said, “but I would say every one of us is more vulnerable.” The unvaccinated are still the most vulnerable by far, especially to more severe outcomes. But even this far into the pandemic, it’s hard to know exactly why some vaccinated and boosted people have gotten sick while others haven’t—good pandemic behaviors might come into play, along with luck. Scientists are still investigating the role of other factors, including whether genetics might be protecting the immune systems of people who haven’t gotten COVID.

Read: Is BA.5 the ‘reinfection wave’?

Nevertheless, all of the experts argued that COVID virgins should still try to avoid infection. Above all, they should get up-to-date on vaccination and boosters. Once those layers of protection are in place, they should continue to be prudent—especially in crowded, indoor settings—but unless they are medically vulnerable, they don’t have to take more precautions than anyone else, Kim-Farley said.

The guidance for this group is the same as it is for everybody else largely because immunity by infection is protective, but only to an extent. BA.5, for one, seems to be able to reinfect people who were previously sick, sometimes even those who just a few months ago had an earlier version of Omicron. At this point, an infection from a year ago, let alone two, might not mean much immunologically. “People shouldn’t rely on prior infection, because it just is not as effective as prior vaccination,” Kim-Farley said. And though “hybrid immunity”—which results when a person gets sick and is then vaccinated, or vice versa—is thought to confer a good amount of protection, “that kind of assertion may be challenged” now that so many reinfections are occurring, the Yale epidemiologist Albert Ko told me.

The ultimate problem with people viewing themselves as sitting ducks is that this is the exact attitude epidemiologists do not want us to have. It can foster a “why bother?” demeanor, negating all public-health efforts to stop transmission and discouraging personal efforts to protect oneself. In other words, it promotes COVID fatalism, which is appealing because it offers relief from the daily anxiety and behavioral compromises of pandemic life by assuming that an infection is a question of when, not if. This notion can be liberating for those who have never gotten infected—and presumably it is part of the reason so few are left: Many people have already adopted a “meh” attitude toward COVID, not letting the fear of an infection get in the way of living their lives.

Even this late in the game, you should really try to avoid getting COVID if you can. Having to take precautions can be frustrating after so many months of pandemic life, but getting sick can be extremely unpleasant, even if you are vaccinated and boosted. There’s the risk of long COVID, yes, but those who escape it can still feel terrible for several days, if not weeks, Bright said. These infections don’t usually lead to hospitalization or death, but they’re no walk in the park either, especially for the elderly and the immunocompromised. And as COVID continues to mutate, you definitely want to forestall a second infection, or a third down the line. The consequences of repeated infections and their potential to cause long COVID or other health issues are not yet known. And, of course, the tenets of COVID 101 are still true: Even if your infection is mild, you can still spread it to someone who could have it much worse.

The grim reality is that as long as the virus shows no signs of abating, the number of COVID virgins will continue to shrink. Grappling with this reality will be a lot less stressful if we reframe the way we talk about getting COVID. Instead of fretting about the virus as something that could come for you, focus on what to do when it does. Those who are vaccinated and boosted may still be ducks sitting in the crosshairs of infection, but in all likelihood they won’t die or get severely ill, especially if they are young and healthy. “That’s what we care most about,” Ko said. The people who haven’t gotten sick should remember that they have already won—vaccines, in tandem with the treatments that are now available, mean that it’s far better to get sick now than it was a year or two ago.

When I told my fiancé that he would probably get COVID but should definitely still try not to get COVID, he described the situation as “Kafkaesque.” Indeed, these are absurd and illogical times. But at the very least, focusing on what is within our control can help us regain a modicum of sense. Short of total isolation, people may not be able to do much to avoid the coronavirus forever, but there’s still plenty they can do to escape the worst when it does come for them.

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

After two years of avoiding the coronavirus, Carrington felt sure that her time had come: She’d been holding her great-niece, who tested positive soon after, “and she was giving me kisses,” Carrington told me. But she never caught the bug. “And I just thought, Wow, I might really be resistant here.” She wasn’t thinking about immunity, which she had thanks to multiple doses of a COVID vaccine. Rather, perhaps via some inborn genetic quirk, her cells had found a way to naturally repel the pathogen’s assaults instead.

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

Read: America is running out of ‘COVID virgins’

The idea of coronaviral resistance is beguiling enough that scientists around the world are now scouring people’s genomes for any hint that it exists. If it does, they could use that knowledge to understand whom the virus most affects, or leverage it to develop better COVID-taming drugs. For individuals who have yet to catch the contagion—a fast-dwindling proportion of the population—resistance dangles “like a superpower” that people can’t help but think they must have, says Paula Cannon, a geneticist and virologist at the University of Southern California.

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

---

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

The HIV-blocking mutation is maybe the most famous. About three decades ago, researchers, Carrington among them, began looking into a small number of people who “we felt almost certainly had been exposed to the virus multiple times, and almost certainly should have been infected,” and yet had not, she told me. Their superpower was simple: They lacked functional copies of a gene called CCR5, which builds a cell-surface protein that HIV needs in order to hack its way into T cells, the virus’s preferred human prey. Just 1 percent of people of European descent harbor this mutation, called CCR5-Δ32, in two copies; in other populations, the trait is rarer still. Even so, researchers have leveraged its discovery to cook up a powerful class of antiretroviral drugs, and purged the virus from two people with the help of Δ32-based bone-marrow transplants—the closest that medicine has come to developing a functional HIV cure.

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

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

Read: Is BA.5 the ‘reinfection wave?’

A full analogue to the HIV, malaria, and norovirus stories may not be possible. Genuine resistance can manifest in only so many ways, and tends to be born out of mutations that block a pathogen’s ability to force its way into a cell, or xerox itself once it’s inside. CCR5, Duffy, and the sugars dropped by FUT2, for instance, all act as microbial landing pads; mutations rob the bugs of those perches. If an equivalent mutation exists to counteract SARS-CoV-2, it might logically be found in, say, ACE2, the receptor that the coronavirus needs in order to break into cells, or TMPRSS2, a scissors-like protein that, for at least some variants, speeds the invasive process along. Already, researchers have found that certain genetic variations can dial down ACE2’s presence on cells, or pump out junkier versions of TMPRSS2—hints that there could be tweaks that further strip away the molecules. But “ACE2 is very important” to blood-pressure regulation and the maintenance of lung-tissue health, said Su, of NIAID, who’s one of many scientists collaborating with Casanova to find SARS-CoV-2 resistance genes. A mutation that keeps the coronavirus out might very well “muck around with other aspects of a person’s physiology.” That could make the genetic tweak vanishingly rare, debilitating, or even, as Gupta put it, “not compatible with life.” People with the CCR5–Δ32 mutation, which halts HIV, “are basically completely normal,” Cannon told me, which means “HIV kind of messed up in ‘choosing’ CCR5.” The coronavirus, by contrast, has figured out how to exploit something vital to its host—an ingenious invasive move.

The superpowers of genetic resistance can have other forms of kryptonite. A few strains of HIV have figured out a way to skirt around CCR5, and glom on to another molecule, called CXCR4; against this version of the virus, even people with the Δ32 mutation are not safe. A similar situation has arisen with Plasmodium vivax, which “we do see in some Duffy-negative individuals,” suggesting that the parasite has found a back door, says Dyann Wirth, a malaria researcher at Harvard’s School of Public Health. Evolution is a powerful strategy—and with SARS-CoV-2 spewing out variants at such a blistering clip, “I wouldn’t necessarily expect resistance to be a checkmate move,” Cannon told me. BA.1, for instance, conjured mutations that made it less dependent on TMPRSS2 than Delta was.

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

Still, protection doesn’t have to be all or nothing to be a perk. Partial genetic resistance, too, can reshape someone’s course of disease. With HIV, researchers have pinpointed changes in groups of so-called HLA genes that, through their impact on assassin-like T cells, can ratchet down people’s risk of progressing to AIDS. And a whole menagerie of mutations that affect red-blood-cell function can mostly keep malaria-causing parasites at bay—though many of these changes come with “a huge human cost,” Wirth told me, saddling people with serious clotting disorders that can sometimes turn lethal themselves.

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

If resistance doesn’t pan out, that doesn’t have to be a letdown. People don’t need total blockades to triumph over microbes—just a defense that’s good enough. And the protection we’re born with isn’t all the leverage we’ve got. Unlike genetics, immunity can be easily built, modified, and strengthened over time, particularly with the aid of vaccines. Those DIY defenses are probably what kept Carrington’s case of COVID down to “a mild course,” she told me. Immune protection is also a far surer bet than putting a wager on what we may or may not inherit at birth. Better to count on the protections we know we can cook up ourselves, now that the coronavirus is clearly with us for good.

When the original Omicron variant swept across the country this winter, it launched America into a new COVID era, one in which nearly everyone—95 percent of adults, according to one CDC estimate—has some immunity to the virus through vaccines, infection, or both. Since then, however, Omicron subvariants have still managed to cause big waves of infection. They’ve accomplished this by eroding our existing immunity.

This will keep happening. “There’s not a lot of things I’m confident about in SARS-CoV-2 evolution, but I think I’m extremely confident we’ll keep seeing new variants that are progressively eroding antibody neutralization,” says Jesse Bloom, an evolutionary virologist at the Fred Hutchinson Cancer Center. Experts are cautiously optimistic that the pace of variant emergence will eventually slow, and for many people, reinfections are already milder and hospitals are not overwhelmed. But as the virus keeps changing, the only real guarantee is that it will be different—and that its changes won’t necessarily affect everyone uniformly.

SARS-CoV-2’s evolution follows a well-understood dynamic: When a variant sweeps around the world, it leaves behind a lot of immunity against itself. This puts intense evolutionary pressure on the virus to change things up; any subsequent variant has to somehow evade immunity to previous variants to keep finding new hosts. There are no limits to how long the coronavirus can keep doing this. Long-established respiratory viruses that cause the flu and common cold are still evolving to keep reinfecting us again and again.

But immune escape isn’t an intrinsic property of any new variant. SARS-CoV-2 is not ascending a ladder with each variant, becoming more and more immune escape-y over time. Rather, think of the coronavirus as an indefatigable rabbit being chased by our immune system, an equally indefatigable dog. The rabbit is always running away from the dog, and the dog is always trying to catch up to the rabbit. The space in which they have to chase each other is so big that it might as well be infinite on human timescales. As Bloom told me previously, the number of possible mutations in SARS-CoV-2 far, far exceeds the number of atoms in the known universe.

Read: You are going to get COVID again … and again … and again.

Occasionally, the rabbit might make a dramatic Omicron-like leap and shoot out ahead for a while until our immunity catches up. How often this will happen is difficult to predict. “It probably depends on how much of a black-swan event Omicron was,” says Adam Lauring, a virologist at the University of Michigan. Omicron was so different and so unusual compared with everything that had come before. “Could it happen again? Most people think probably not but … you don’t want to be burned twice.” Whether an Omicron-like event happens every two or 20 or 200 years can mean different trajectories for COVID’s future. But at this point, we have only two and a half years of data to go on, so prognosticate at your own risk.

More predictably, though, SARS-CoV-2 is likely to make smaller gains over time, accumulating mutations that make it incrementally better at reinfection. Virologists call this “antigenic evolution.” (Antigenic refers to the parts of a pathogen recognized by our immune system. For SARS-CoV-2, this is predominantly the spike protein.) Different viruses do seem capable of different rates of antigenic evolution. Of the four seasonal coronaviruses that cause common colds, for example, OC43 and 229E are evolving at a rate of 0.3 to 0.5 adaptive mutations in their spike proteins each year. But a third, NL63, doesn’t seem to be changing much at all, says Kathryn Kistler, a virologist also at Fred Hutch who has studied the evolution of the seasonal coronaviruses. She is currently trying to confirm this with blood-serum samples collected in the ’80s and ’90s. And there are so few samples of the fourth coronavirus, HKU1, that we don’t have enough to discern any trend.

Influenza is much better studied, and different types of flu also exhibit different rates of evolution from one another. Of the most common ones, influenza B is the slowest, roughly on par with the coronaviruses OC43 and 229E. H1N1 flu is faster, and H3N2, the predominant flu strain in the world right now, is the fastest. The differences may, at least in part, come down to the shape of the antigen that our immune system recognizes. The spike protein in coronaviruses, for example, needs to change enough so it fools the immune system, but not so much that it stops functioning altogether. H3N2 can get away with a smaller change in its spike-protein analogue: “It’s often one single mutation—sometimes two—[that] can give the virus a huge advantage,” Kistler told me.

Contrast that with measles, a virus that has barely evolved over decades. Our antibodies recognize multiple parts of its key protein. A recent study found that at least five out of eight key sites of that protein need to change at once to erode our immune defenses. A mutation in only one or two of these sites doesn’t confer much of an advantage, but gaining all five at once is very unlikely. So any potential new variants fizzle out, and the dominant measles variant stays quite stable.

Read: Is BA.5 the ‘reinfection wave’?

SARS-CoV-2, though, has been evolving antigenically faster than any of these viruses, even faster than H3N2. This could come down to the uniqueness of its spike protein, but some of this unusually fast pace over the past two years probably also has to do with the virus being novel. When a new strain of H1N1 “swine flu” hit in 2009, Kistler pointed out, it, too, had an initial burst before slowing down. The coronavirus’s Alpha and Delta variants emerged during a time with many immunologically naive people to infect, and the earliest variants mostly succeeded by becoming more intrinsically transmissible. The virus can only increase its transmissibility by so much, Bloom says, so SARS-CoV-2 is going to have less and less room to improve. However, it can keep finding new ways to get around immunity, as the Omicron subvariants have been doing.

The immunity landscape that SARS-CoV-2 is evolving against is also changing, though. Right now, some people have immunity against the original coronavirus or Alpha or Delta, others have immunity against the Omicron family, and yet others have both. As more variants emerge, our individual exposure history is going to be even more heterogeneous; depending on our previous immunity, some of us might be more susceptible than others to a new variant. The impact will be less uniform. We’ve already seen this with the Omicron subvariants, where countries with smaller previous waves are experiencing bigger BA.5 waves. Some people will also experience more waning immunity than others; older people, for example, tend to mount less durable immune responses to SARS-CoV-2, which is why this group is always prioritized for boosters. Aggressive vaccine updates and booster campaigns would help everyone’s immune system keep up.

Instead of always trying to catch up to the virus though, could we broaden our immunity and get ahead of it? Our current vaccines, while still very good at protecting against severe disease, are not capable of this. The White House is now promoting—though not really funding—next-generation vaccines that could potentially do better: pan-coronavirus vaccines that scientists hope will elicit antibodies against parts of the spike protein that do not change very much, or nasal vaccines to elicit antibodies in the nose and mouth where the virus first replicates, perhaps stopping an infection altogether.

But these ideas are not new to SARS-CoV-2—researchers have been trying these approaches to flu for many years. A universal flu vaccine is still elusive. A nasal flu vaccine, FluMist, does exist, but its effectiveness is quite mixed: It was originally thought to be more effective than the shot, then believed to be less effective—so much so that the CDC pulled the vaccine from 2016 to 2018—until it was reformulated. In any case, it’s clear that FluMist doesn’t come close to preventing all mild flu infections. Barring any major innovations in vaccine technology, our immune systems may be the dog chasing the coronavirus rabbit for a long time still.

When the monkeypox outbreak was first detected in the United States, it seemed, as far as infectious-disease epidemics go, like one this country should be able to handle. Tests and antivirals for the virus already existed; the government had stockpiled vaccines. Unlike SARS-CoV-2, monkeypox was a known entity, a relative softball on the pathogenic field. It wasn’t hypertransmissible, moving mainly through intimate contact during the disease’s symptomatic phase; previous epidemics had, with few interventions, rather quickly burned themselves out. The playbook was clear: Marshal U.S. resources and ensure they go to those most at risk, send aid abroad, and knock it out of the park. “If there was one virus that would lend itself to containment,” says Boghuma Kabisen Titanji, a virologist and infectious-disease physician at Emory University, this should have been it.

Two months later, global counts have crested above 21,000 confirmed cases, nearly a fourth of which are in the United States, which now ranks first among countries keeping track. Infections, most among men who have sex with men, have been documented in 46 states, D.C., and Puerto Rico; New York State and San Francisco have declared the outbreak a health emergency, as has the World Health Organization, on a global scale. Controlling the virus isn’t yet out of reach, says Jay Varma, the director of the Cornell Center for Pandemic Prevention and Response. But as the outbreak grows, so, too, does the challenge of combatting it. “It didn’t have to be this hard,” Varma told me.

Years of similar snafus surrounding SARS-CoV-2—a far, far more difficult virus to fight—should have taught the U.S. something about its own weak points. Instead, the lackluster response to monkeypox is making clear that the country’s capacity to deal with infectious disease may be even worse than it was at the start of 2020. Monkeypox, the country’s second infectious crisis in three years, isn’t just an unfortunate fumble. It’s confirmation that, although the U.S. might have once seemed like one of the nations best equipped to stop and prevent outbreaks, it is, in actuality, one of the best at squandering its potential instead.

---

For years, the warning signs about monkeypox have been there. Decades of sporadic outbreaks in Central and West Africa had made the virus’s toll clear: It can cause a painful, debilitating sickness, with bouts of fevers and rashes, and in numerous cases leaves permanent scars behind; on occasion, certain strains of the pathogen can even kill. And though in many places the virus has infected indiscriminately, striking communities in close physical proximity to wildlife, a 2017 outbreak among young men in Nigeria hinted that sex could pose a particular risk.

So when case numbers began to erupt in several parts of Europe in May, indicating that the epidemic was already widespread, “it should have been obvious” that the epidemic had massive potential to expand, Varma told me. Multiple nations were already involved; the upcoming summer travel season posed a high risk. Infections were also concentrating in communities of men who have sex with men—networks that sexual-health experts know to be “dense, and where infectious diseases propagate very fast,” he said. And still, amid ringing alarm bells, the United States “underreacted,” Varma said, again and again.

Read: We should have seen monkeypox coming

Through much of May and June, monkeypox tests remained siloed within the CDC and its network of public-health labs, already stretched by the pandemic response. Health-care providers had to shuttle specimens to these centers for diagnosis, leaving patients on tenterhooks for days, even weeks, and delaying treatment, vaccination, and contact tracing. Even now, after testing capacity has climbed with the help of commercial labs, typical result turnaround times are stretching long. In Missouri, for instance, “they’re still telling us three to four days” at best, Hilary Reno, the medical director of the St. Louis County Sexual Health Clinic, told me.

Shots, too, have been troublingly scarce. America’s strategic national stockpile has millions of doses of smallpox vaccine (which also works against monkeypox), but most are ACAM2000, an inoculation that’s been linked to rare but serious side effects and shouldn’t be taken by certain vulnerable groups, including people living with HIV. Another shot, branded as Jynneos in the U.S., is safer, though, as a two-doser, may be trickier to administer post-exposure. Since spring, manufacturers of this shot have been turning the crank on assembly lines to bolster supply. But American officials hemmed and hawed for weeks before flying in much-needed doses from abroad, and then only in spurts.

The issue at hand certainly isn’t about vaccine demand. “Evey gay man I know is very ready for this vaccine and is willing to stand in line to get it,” says Steven Thrasher, a journalist and the author of The Viral Underclass, which examines the intersection of infectious disease and social inequality. Even though more vaccine doses are headed out, however, as cases balloon, the country still might not have enough. And with testing still strained, it won’t necessarily send doses to the right places. In Missouri, for instance, only a handful of cases has been reported so far, Reno told me. But with plenty of transmission likely going undetected, the state’s original order of shots might not cover its true needs. The country dawdled so long at the start line that even the relatively slow-moving monkeypox took its chance to race ahead—leaving the gap more and more difficult to close.

Early shortages in testing and care have also made the scope of the American outbreak difficult to estimate, or communicate—another parallel to the botched COVID response. A lack of tests means a lack of accurate numbers, which can make a devastating epidemic look deceptively contained. “That amplifies the cycle of neglect,” Varma told me, a pattern to which the U.S. has been particularly prone. Piling on to the problem is the ongoing dearth of funds for America’s sexual-health services, coincident with a recent rise in STIs. People with genital symptoms have struggled to reach providers, opening up even more cryptic channels for the virus to spread through.

Monkeypox is also a particularly challenging outbreak to be grappling with in the U.S., where sex is still a polarizing taboo, and men who have sex with men remain a marginalized community. And this is an especially charged time to be discussing the LGBTQ community in America, as the recent rolling back of abortion protections has stoked anxiety that other federal civil liberties may soon be on the chopping block. “We’re at this profoundly anti-gay, anti-trans moment,” Thrasher told me, at a time when those communities need more protection, not less.

Experts have praised some of the CDC’s efforts to avoid stigmatizing at-risk groups, which, at this juncture, remains essential. Monkeypox certainly doesn’t need sex to spread, Ina Park, a sexual-health expert at UC San Francisco, told me. Kissing, cuddling, and other situations that put bodies in close proximity for prolonged periods can also transmit the virus. So can contact with clothing or bed linens, because monkeypox can persist on unsanitized surfaces for days. Which does mean that men who have sex with men are definitely not the only ones in danger. At the same time, some people have been so fearful of casting monkeypox as an exclusively “gay disease” that sex has almost been censored from discussions, “giving people a misperception of the different risks that populations are facing right now,” Thrasher said. Especially while supplies remain so limited, we need to be “vaccinating people where the virus is moving.” Which means “we need to give both messages simultaneously,” Park said, “that this is not something that only affects gay men” while nodding to the fact that monkeypox is still “primarily affecting certain communities,” a trend that should influence the distribution of shots. Calls for the mass vaccination of “children or cis-het suburban moms,” Titanji told me, are “not where you’re going to get the most impact.”

Read: U.S. messaging on monkeypox is deeply flawed

To communities of men who have sex with men, how the Biden administration acts in this moment is revealing unspoken priorities and values. “In June, when it’s time to put rainbow flags up, they do,” says Keletso Makofane, an epidemiologist at Harvard’s School of Public Health, who’s been tracking the outbreak’s progression via an LGBTQ-community-led survey. “But when it’s time to give us resources? To prevent what some people describe as the worst pain they’ve ever felt in their lives? They choose not to.” Now, some experts are even bogged down in debates over whether monkeypox should be described as a sexually transmitted infection. But underlying the squabble is the far more important question of resource allocation, Makofane told me. This is “really a conversation about, Do these people deserve compassion and care?” Continuing to draw vital tools and resources away from at-risk populations, he said, would suggest the nation believes that the answer is no.

As long as the virus continues to move predominantly through networks of men who have sex with men, the U.S. still has the opportunity to swiftly intervene, track transmission, and dole out resources in a targeted way, Varma told me. But monkeypox’s current pattern may not hold. Already, the virus has begun to hop across genders and age groups, leveraging other, nonsexual forms of close contact. Infections in young children, who likely contracted the infection in their households, and among people incarcerated in prisons, where contagion is particularly difficult to quash, are starting to appear. And across geographies, familiar inequities in access to tests, vaccines, and treatments have begun to appear.

Monkeypox’s overlapping tenure with SARS-CoV-2 has aggravated matters as well. “This virus could not have picked a worse time to make its grand entrance to the global scene,” Titanji said. Still reeling from one outbreak, people are weary, and have “very little appetite for taking on another,” Thrasher told me. Numbed by COVID’s persistent toll, the public has also latched onto comforting comparisons that, although based in kernels of truth, have been warped into misleading extremes: Monkeypox might be less transmissible and less deadly than the coronavirus, but it is not an ignorable nuisance that’s guaranteed to dissipate. The larger the swath of society that’s affected, Titanji told me, the unwieldier the outbreak gets.

The top priority now, experts told me, should be funneling funds toward distributing vaccines and scaling up testing. Health workers and patients need continued guidance on the disease’s often-subtle symptoms and the possibility of silent transmission, as well as the resources to administer speedy care. Paid sick leave and housing support would also help ease the burden of monkeypox isolation, which, given the lengthy course of symptoms, can last for weeks. Should such efforts fall short, as they clearly have with SARS-CoV-2, monkeypox could become the second virus to set up permanent residence in the U.S. in the span of three years—giving it all the more opportunity to find new ways to spread, shape-shift, and propagate disease. Preventing that means acting decisively now, to make up for the time we’ve already lost.