Sick Woman Lying In Bed With Tissues (Getty Images/Obradovic)
SARS-CoV-2, the virus that causes COVID, is devastating precisely because it can worm its way into so many different organs and systems in the body. That manifests as different symptoms, from fever to trouble breathing, although an infection can be asymptomatic, too — that is, no symptoms at all.
Throughout the pandemic, there have been a few telltale signs of COVID infection. The loss of sense of smell and taste were chief among them. But as the virus has mutated again and again, creating new strains like Typhon (BQ.1) and Gryphon (XBB) which can evade some of our tools to fight it, it seem that the symptoms of COVID may have changed as well.
Recent estimates published by the Centers for Disease Control and Prevention on Friday pegged Typhon and its close relative Cerberus (BQ.1.1) as making up 27 percent of cases, an 11 percent increase from last week. Meanwhile, cases of BA.5, the strain that has dominated cases for the majority of summer, dipped below 50 percent for the first time in months.
Indeed, emerging data suggests the symptoms of COVID are changing with new variants. And, they can differ regardless of whether you’ve been vaccinated or not, or previously infected. Newly released data from the ZOE Health Study, which maintains the COVID Symptom Tracker app, finds that the dominant symptoms have shifted.
The app was originally launched in March 2020. It quickly logged one million users, who typed in how COVID was making them feel, allowing researchers to pin down some of the most common COVID symptoms. It was part of the reason why it became well-known that anosmia (loss of smell and taste) is a key symptom of the original COVID strain.
More recently, ZOE crunched the data from over 4.8 million users and found that after two vaccinations, the top-ranking symptoms were sore throat, runny nose, blocked nose, persistent cough, headache, in that order. (Vaccines can protect against severe disease, which generally means hospitalization or death, but breakthrough infections are not unheard of, although far less severe than infections in the unvaccinated.)
Loss of smell has slipped to the number nine slot, while shortness of breath is down at number 30 for this group. ZOE says this indicates “the symptoms as recorded previously are changing with the evolving variants of the virus.”
Just one dose of a vaccine can shift the order of most common symptoms to headache, runny nose, sore throat, sneezing and then persistent cough. For those who haven’t received a vaccine at all, the symptoms are generally closer to the original ranking from 2020: headache, sore throat, runny nose, fever and persistent cough.
However, loss of smell has slipped to the number nine slot, while shortness of breath is down at number 30 for this group. ZOE says this indicates “the symptoms as recorded previously are changing with the evolving variants of the virus.”
Just because SARS-2 appears to be evolving does not mean that it will become more “mild” — and it’s definitely nothing like the flu or a regular cold. The virus indiscriminately attacks the inner lining of blood vessels, causing injuries to the heart and lungs, and can cause literal brain damage. Given the broad range of debilitating symptoms known as long COVID, it doesn’t really make sense to call this “mild.”
Additionally, repeat infections could have unknown consequences — experts aren’t entirely sure what happens when you get COVID two, three or more times. That’s why watching out for new symptoms are so important. COVID may manifest differently because different viral strains sometimes impact different parts of the body. The delta strain, for example, found its niche in the lower respiratory tract, while omicron BA.2 tends to prefer the upper airway.
But it’s also critical to note that the data from ZOE is self-reported and doesn’t take into account demographic information or which variant caused the infection. It’s also using averages to report the most common symptoms — everyone is different and there is no guarantee here the disease will follow a certain course.
Nonetheless, the data gives a good idea of what to expect and people should be aware of these changes in order to best protect themselves. And the tools to fight COVID haven’t really changed: testing, masking, indoor ventilation, drugs like Paxlovid and, of course, the vaccines are all powerful strategies we should be using more to prevent this winter wave from becoming extremely deadly.
The Biden Administration warned this week that an estimated 30–70,000 Americans could die from the virus this winter. But even a small wave could cause supply chain disruptions and sicken millions. One thing that could make this winter worse than previous COVID waves is the rise of a “variant soup,” meaning multiple new strains of the virus surging at once.
In previous fall and winter waves, only one type of the virus (i.e. delta or the original “wild type” strain) has really dominated. Public health experts are also warning of a “twindemic” or even “tripledemic” in which COVID surges along with flu and respiratory syncytial virus (RSV). Most people may have never heard of RSV, but it was first discovered in chimpanzees in 1956, and the virus regularly causes outbreaks in humans.
It’s usually only serious in babies and older people, but it’s still not a fun illness. Even though the fall is just beginning, both flu and RSV are returning with a vengeance after relatively few cases the previous two years. On Friday, the Washington Post reported that this flu season is early and more severe than it has been in 13 years, “with at least 880,000 cases of influenza illness, 6,900 hospitalizations and 360 flu-related deaths nationally.”
Meanwhile, pediatric hospital beds across the U.S. are filling up with RSV cases, many of them completely full for weeks. Symptoms of flu and RSV may overlap (cold-like symptoms like fever, runny nose, coughing), making it somewhat confusing for sick people to know what illness they really have. That underscores the importance of testing for COVID and visiting a doctor when ill, if you have access to medical care. It also serves as a reminder to stay home when sick and mask up when possible.
Masking prevents the spread of all three of these viruses: flu, RSV and COVID. That’s one theory as to why the last two winters have been mostly free of diseases other than COVID, which has dominated due to its novelty and severe contagiousness. But as restrictions loosen, some of these more familiar viruses are coming roaring back. Keeping track of new and old symptoms is really only part of the equation. Masks, vaccines and social distancing continue to be some of the best tools at our disposal.
Only a couple dozen doctors specialize in chronic fatigue syndrome (ME/CFS). Now their knowledge could be crucial to treating millions more patients. Kira Stoops lives in Bozeman, Montana—a beautiful mountain town where it sometimes feels like everyone regularly goes on 50-mile runs. Stoops, however, can’t walk around her own block on most days. To stand for more than a few minutes, she needs a wheeled walker.
She reacts so badly to most foods that her diet consists of just 12 ingredients. Her “brain fog” usually lifts for a mere two hours in the morning, during which she can sometimes work or, more rarely, see friends. Stoops has myalgic encephalomyelitis, or chronic fatigue syndrome (ME/CFS). “I’m considered a moderate patient on the mild side,” she told me.
ME/CFS involves a panoply of debilitating symptoms that affect many organ systems and that get worse with exertion. The Institute of Medicine estimates that it affects 836,000 to 2.5 million people in the U.S. alone, but is so misunderstood and stigmatized that about 90 percent of people who have it have never been diagnosed.
At best, most medical professionals know nothing about ME/CFS; at worst, they tell patients that their symptoms are psychosomatic, anxiety-induced, or simply signs of laziness. While ME/CFS patients, their caregivers, and the few doctors who treat them have spent years fighting for medical legitimacy, the coronavirus pandemic has now forced the issue.
Even if that proportion is 10 times lower for SARS-CoV-2, the number of Americans with ME/CFS would still have doubled in the past three years. “We’re adding an immense volume of patients to an already dysfunctional and overburdened system,” Beth Pollack, a scientist at MIT who studies complex chronic illnesses, told me.
The U.S. has so few doctors who truly understand the disease and know how to treat it that when they convened in 2018 to create a formal coalition, there were only about a dozen, and the youngest was 60. Currently, the coalition’s website lists just 21 names, of whom at least three have retired and one is dead, Linda Tannenbaum, the CEO and president of the Open Medicine Foundation, told me.
These specialists are concentrated on the coasts; none work in the Midwest. American ME/CFS patients may outnumber the population of 15 individual states, but ME/CFS specialists couldn’t fill a Major League Baseball roster.
Stoops, who is 39, was formally diagnosed with ME/CFS only four years ago, and began receiving proper care from two of those specialists—Lucinda Bateman of the Bateman Horne Center and David Kaufman from the Center for Complex Diseases. Bateman told me that even before the pandemic, she could see fewer than 10 percent of the patients who asked for a consultation. “When I got into those practices, it was like I got into Harvard,” Stoops told me.
ME/CFS specialists, already overwhelmed with demand for their services, now have to decide how to best use and spread their knowledge, at a time when more patients and doctors than ever could benefit from it. Kaufman recently discharged many of the more stable ME/CFS patients in his care—Stoops among them—so that he could start seeing COVID long-haulers who “were just making the circuit of doctors and getting nowhere,” he told me.
“I can’t clone myself, and this was the only other way to” make room for new patients. Bateman, meanwhile, is feverishly focused on educating other clinicians. The hallmark symptom of ME/CFS—post-exertional malaise, or PEM—means even light physical or mental exertion can trigger major crashes that exacerbate every other symptom. Doctors who are unfamiliar with PEM, including many now running long-COVID clinics, can unwittingly hurt their patients by encouraging them to exercise.
Bateman is racing to spread that message, and better ways of treating patients, but that means she’ll have to reduce her clinic hours. These agonizing decisions mean that many existing ME/CFS patients are losing access to the best care they had found so far—what for Stoops meant “the difference between being stuck at home, miserable and in pain, and actually going out once or twice a day, seeing other humans, and breathing fresh air,” she told me.
But painful trade-offs might be necessary to finally drag American medicine to a place where it can treat these kinds of complex, oft-neglected conditions. Kaufman is 75 and Bateman is 64. Although both of them told me they’re not retiring anytime soon, they also won’t be practicing forever. To make full use of their expertise and create more doctors like them, the medical profession must face up to decades spent dismissing illnesses such as ME/CFS—an overdue reckoning incited by long COVID.
“It’s a disaster possibly wrapped up in a blessing,” Stoops told me. “The system is cracking and needs to crack.” Many ME/CFS specialists have a deep knowledge of the disease because they’ve experienced it firsthand. Jennifer Curtin, one of the youngest doctors in the field, has two family members with the disease, and had it herself for nine years. She improved enough to make it through medical school and residency training, which showed her that ME/CFS “just isn’t taught,” she told me. Most curricula don’t include it; most textbooks don’t mention it.
Even if doctors learn about ME/CFS, America’s health-care system makes it almost impossible for them to actually help patients. The insurance model pushes physicians toward shorter visits; 15 minutes might feel luxurious. “My average visit length is an hour, which doesn’t include the time I spend going over the patient’s 500 to 1,700 pages of records beforehand,” Curtin said. “It’s not a very scalable kind of care.” (She works with Kaufman at the Center for Complex Diseases, which bills patients directly.)
This also explains why the cohort of ME/CFS clinicians is aging out, with little young blood to refresh them. “Hospital systems want physicians to see lots of patients and they want them to follow the rules,” Kaufman said. “There’s less motivation for moving into areas of medicine that are more unknown and challenging.”
ME/CFS is certainly challenging, not least because it’s just “one face of a many-sided problem,” Jaime Seltzer, the director of scientific and medical outreach at the advocacy group MEAction, told me. The condition’s root causes can also lead to several distinct but interlocking illnesses, including mast cell activation syndrome, Ehlers-Danlos syndrome, fibromyalgia, dysautonomia (usually manifesting as POTS), and several autoimmune and gastrointestinal disorders.
“I’m still amazed at how often patients come in with Complaint No. 1, and then I find five to seven of the other things,” Kaufman said. These syndromes collectively afflict many organ systems, which can baffle doctors who’ve specialized in just one. Many of them disproportionately affect women, and are subject to medicine’s long-standing tendency to minimize or psychologize women’s pain, Pollack told me:
An average woman with Ehlers-Danlos syndrome typically spends 16 years getting a diagnosis, while a man needs only four. People with long COVID might have many of these conditions and not know about any—because their doctors don’t either. Like ME/CFS, they rarely feature in medical training, and it’s hard to “teach someone about all of them when they’ve never heard of any of them,” Seltzer said.
Specialists like Bateman and Kaufman matter because they understand not just ME/CFS but also the connected puzzle pieces. They can look at a patient’s full array of symptoms and prioritize the ones that are most urgent or foundational. They know how to test for conditions that can be invisible to standard medical techniques: “None of my tests came back abnormal until I saw an ME/CFS doctor, and then all my tests came back abnormal,” said Hannah Davis of the Patient-Led Research Collaborative, who has had long COVID since March 2020.
ME/CFS specialists also know how to help, in ways that are directly applicable to cases of long COVID with overlapping symptoms. ME/CFS has no cure but can be managed, often through “simple, inexpensive interventions that can be done through primary care,” Bateman told me. Over-the-counter antihistamines can help patients with inflammatory problems such as mast cell activation syndrome. Low doses of naltrexone, commonly used for addiction disorders, can help those with intense pain.
A simple but rarely administered test can show if patients have orthostatic intolerance—a blood-flow problem that worsens other symptoms when people stand or sit upright. Most important, teaching patients about pacing—carefully sensing and managing your energy levels—can prevent debilitating crashes. “We don’t go to an ME/CFS clinic and walk out in remission,” Stoops told me. “You go to become stabilized. The ship has 1,000 holes, and doctors can patch one before the next explodes, keeping the whole thing afloat.”
That’s why the prospect of losing specialists is so galling. Stoops understands why her doctors might choose to focus on education or newly diagnosed COVID long-haulers, but ME/CFS patients are “just so lost already, and to lose what little we have is a really big deal,” she said. Kaufman has offered to refer her to generalist physicians or talk to primary-care doctors on her behalf. But it won’t be the same: “Having one appointment with him is like six to eight appointments with other practitioners,” she said.
He educates her about ME/CFS; with other doctors, it’s often the other way round. “I’m going to have to work much harder to receive a similar level of care.” At least, she will for now. The ME/CFS specialists who are shifting their focus are hoping that they can use this moment of crisis to create more resources for everyone with these diseases. In a few years, Bateman hopes, “there will be 100 times more clinicians who are prepared to manage patients, and many more people with ME/CFS who have access to care.”
For any mainstream disease, such events—a report, a guideline revision, a review article—would be mundane. For ME/CFS, they felt momentous. And yet, “the current state of things is simply intolerable,” Julie Rehmeyer, a journalist with ME/CFS, told me. Solving the gargantuan challenge posed by complex chronic diseases demands seismic shifts in research funding, medical training, and public attitudes. “Achieving shifts like that takes something big,” Rehmeyer said. “Long COVID is big.”
COVID long-haulers have proved beyond any reasonable doubt that acute viral infections can leave people chronically ill. Many health-care workers, political-decision makers, and influencers either know someone with long COVID or have it themselves. Even if they still don’t know about ME/CFS, their heightened awareness of post-viral illnesses is already making a difference. Mary Dimmock’s son developed ME/CFS in 2011, and before the pandemic, one doctor in 10 might take him seriously.
“Now it’s the flip: Only one doctor out of 10 will be a real jerk,” Dimmock told me. “I attribute that to long COVID.” But being believed is the very least that ME/CFS patients deserve. They need therapeutics that target the root causes of the disease, which will require a clear understanding of those causes, which will require coordinated, well-funded research—three things ME/CFS has historically lacked.
But here, too, “long COVID is going to be a catalyst,” Amy Proal, the president of the Polybio Research Foundation, told me. She is leading the Long Covid Research Initiative—a group of scientists, including ME/CFS researchers, that will use state-of-the-art techniques to see exactly how the new coronavirus causes long COVID, and rapidly push potential treatments through clinical trials.
While they wait for better treatments, patients also need the medical community to heed the lessons that they and their clinicians have learned. For example, the American Academy for Family Physicians website still wrongly recommends exercise therapy and links ME/CFS to childhood abuse. “That group of doctors is very important to these patients,” Dimmock said, “so what does that say to them about what this disease is all about?”
Despite all evidence to the contrary, many clinicians and researchers still don’t see ME/CFS as a legitimate illness and are quick to dismiss any connection between it and long COVID. To ensure that both groups of patients get the best possible treatments, instead of advice that might harm them, ME/CFS specialists are working to disseminate their hard-won knowledge.
Bateman and her colleagues have been creating educational resources for cliniciansand patients, continuing-medical-education courses, and an online lecture series. Jennifer Curtin has spent two years mapping all the decisions she makes when seeing a new patient, and is converting those into a tool that other clinicians can use. As part of her new start-up, called RTHM, she’s also trying to develop better ways of testing for ME/CFS and its related syndromes, of visualizing the hefty electronic health records that chronically ill patients accumulate, and of tracking the treatments they try and their effects.
“There are a lot of things that need to be fixed for this kind of care to be scalable,” Curtin told me. Had such shifts already occurred, the medical profession might have had more to offer COVID long-haulers beyond bewilderment and dismissal. But if the profession starts listening to the ME/CFS community now, it will stand the best chance of helping people being disabled by COVID, and of steeling itself against future epidemics.
Pathogens have been chronically disabling people for the longest time, and more pandemics are inevitable. The current one could and should be the last whose long-haulers are greeted with disbelief. New centers that cater to ME/CFS patients are already emerging. RTHM is currently focused on COVID long-haulers but will take on some of David Kaufman’s former patients in November, and will open its waiting list to the broader ME/CFS community in December.
(It is currently licensed to practice in just five states but expects to expand soon.) David Putrino, who leads a long-COVID rehabilitation clinic in Mount Sinai, is trying to raise funds for a new clinic that will treat both long COVID and ME/CFS. He credits ME/CFS patients with opening his eyes to the connection between long COVID and their condition.
Every ME/CFS patient I’ve talked with predicted long COVID’s arrival well before most doctors or even epidemiologists started catching up. They know more about complex chronic illnesses than many of the people now treating long COVID do. Despite having a condition that saps their energy, many have spent the past few years helping long-haulers navigate what for them was well-trodden terrain: “I did barely anything but work in 2020,” Seltzer told me.
Against the odds, they’ve survived. But the pandemic has created a catalytic opportunity for the odds to finally be tilted in their favor, “so that neither patients nor doctors of any complex chronic illness have to be heroes anymore,” Rehmeyer said.
The evasive BA.5 omicron variant is driving up Covid cases and hospitalizations as it spreads rapidly across the United States—but despite deaths remaining lower compared to earlier waves, experts tell Forbes there are still plenty of reasons to remain cautious and warn Americans against letting their guard down too soon.
While Covid-19 cases and hospitalizations have been on the rise in most states in recent weeks and jumped 20% nationwide over the past fortnight, deaths have risen only modestly and have hovered around 300-400 a day since April. Driving the new wave is BA.5, an omicron offshoot that has a “superpower to cause reinfection” and can evade immunity from vaccination and previous infection, even from other omicron variants, Dr. Peter Chin-Hong, an infectious disease expert at the University of California, San Francisco, told Forbes.
The disconnect reflects the fact that vaccines and past infections still provide strong protection against serious illness and death for BA.5 as well as there being more options available to treat early disease like Pfizer’s Paxlovid. Chin-Hong said there are still plenty of reasons to avoid infection, not least because Covid can still cause severe symptoms “even if you don’t end up in the hospital” and symptoms can “last for weeks.”
Infection also carries the risk of “long Covid”—lingering and sometimes debilitating symptoms that can persist for months or years—and early evidence suggests this is more likely the more times you get infected. Avoiding infection also helps safeguard people around you who may have less protection against serious disease like children, the elderly and those with weakened immune systems, Dr. Stuart Turville, a virologist at the University of New South Wales in Australia, told Forbes.
Increasingly transmissible variants of omicron have surged across the U.S. this year. BA.5, the most infectious form of the virus yet, rapidly spread and became the dominant variant in early July. It now accounts for an estimated 78% of cases, according to the Centers for Disease Control and Prevention and community transmission has spiked. Concerns over BA.5, as well as the related BA.4, prompted officials to direct vaccine makers to target the variants in updated shots and the Biden Administration announced new plans to tackle its spread.
Officials and experts say it is especially important to ensure strong protection against serious disease by keeping up-to-date on vaccinations, including booster shots. Despite the appeals of public health officials and being available for many months, booster uptake in the U.S. is poor. Fewer than half of fully vaccinated people have received their first booster dose and fewer than 30% of those who have and are eligible for a second have taken up the offer, according to CDC data.
More variants. It is inevitable that SARS-CoV-2, the virus that causes Covid-19, will evolve and spawn new variants over time. Another omicron offshoot, BA.2.75—inexplicably and successfullydubbed “Centaurus” by the internet—has already caught the eye of virologists. The variant is spreading rapidly in India, has been detected across Europe and North America and shows signs of evading immunity.
Little data is available and it’s not clear whether BA.2.75 causes more severe disease. It’s also not clear whether it would be able to take over from BA.5 “as the ruler of the roost,” Chin-Hong explained, as they haven’t had a chance to directly compete with each other as yet.”
A great deal. Data collection and surveillance is poor compared to earlier on in the pandemic. Individual testing is down, genomic surveillance is reduced and evidence suggests cases could be vastly higher than official figures state. Conversely, hospital figures are inflated and reflect routine testing upon admission, which catches many “incidental” infections from people seeking care for other problems.
There is a lot to be understood about the newer omicron variants as well, experts say. BA.5, as well as other more recent omicron offshoots like BA.4 and BA.2.75, are relatively new pathogens that are infecting or reinfecting large numbers of people in the community, Turville explained, which makes it hard to provide absolute and definitive answers. “As with most things with SARS CoV-2, it is a large bag of unknowns,” he added.
Turville told Forbes the decoupling of deaths from cases shows the longer term effects of vaccination and exposure to the virus. It’s a “maturing immunity to SARS-CoV-2 in general” which has taken off the “edge of disease severity,” he added.
While cases are growing—and likely undercounted—it’s worth noting that they are a long way from the earlier omicron peak in January. In July, there were around 100,000-120,000 cases reported on average compared to more than 800,000 in mid January.
I am a senior reporter for the Forbes breaking news team, covering health and science from the London office. Previously I worked as a reporter for a trade publication
So far there is no evidence that this variant causes more serious illness. And infectious disease experts say that even though new infections are on the rise, the impact of BA.5 is unlikely to be on the scale of the surge we saw last winter — in part because the country is better equipped to manage it.
The U.S. is averaging about 300 deaths a day, compared to 3,000 last winter. Dr. Anna Durbin, a professor at the Johns Hopkins University School of Medicine, says the combination of prior infections and vaccinations is still protective, and COVID-19 treatments are better.
“Most people have some underlying immunity that is helpful in fighting the virus,” she explains. “We have antivirals … And I think that because of that … we’re not seeing a rise in deaths. And that’s very reassuring. It tells me that even this virus, even BA.5, is not so divergent that it is escaping all arms of the immune system.”
She adds that new booster shots specifically targeting omicron — which could roll out as soon as this fall — should also be helpful in preventing serious illness and deaths.
There are steps you can take to reduce your exposure to the virus, like masking up in crowded indoor spaces. Here’s how to step up your mask game.
Americans who haven’t had covid-19 are now officially in the minority. A study published this week from the US Centers for Disease Control and Prevention (CDC) found that 58% of randomly selected blood samples from adults contained antibodies indicating that they had previously been infected with the virus; among children, that rate was 75%.
What is different about that minority of people that hasn’t yet gotten infected? Stories abound of close calls, of situations where people are sure they could have (or should have) gotten sick, but somehow dodged infection. Not all the questions are answered yet, but the question of what distinguishes the never-covid cohort is a growing area of research even as the US moves “out of the full-blown” pandemic. Here are the possibilities that scientists are considering to explain why some people haven’t contracted the virus.
They behave differently
We’ve seen it play out time and time again—some people adhere more strictly to protocols known to reduce transmission of the virus, including wearing a mask and getting vaccinated. Some people avoid large public settings and may have even been doing so before the pandemic, says Nicholas Pullen, a biology professor at the University of Northern Colorado. Then again, that doesn’t tell the whole story; as Pullen himself notes: “Ironically, I happen to be one of those ‘never COVIDers’ and I teach in huge classrooms!”
They’ve trained their immune systems
The immune system, as any immunologist or allergist can tell you, is complicated. Though vaccination against covid-19 can make symptoms more mild for some people, it can prevent others from contracting the illness altogether.
Growing evidence suggests that there may be other ways that people are protected against the virus even without specific vaccines against it. Some could have previously been infected with other coronaviruses, which may allow their immune systems to remember and fight similarly shaped viruses. Another study suggests that strong defenses in the innate immune system, barriers and other processes that prevent pathogens from infecting a person’s body, may also prevent infection.
An innate immune system that’s already not functioning as well due to other medical conditions or lifestyle factors such as sleep or diet may put a person at higher risk of getting sick from a pathogen. There’s not single answer here yet, but initial studies are intriguing and may offer avenues for future treatments for covid-19 and other conditions.
They’re genetically different
In the past, studies have found interesting associations between certain genetic variants and people’s susceptibility to communicable diseases such as HIV, tuberculosis, and the flu. Naturally, researchers wondered if such a variant could exist for covid-19. One June 2021 study that was not peer reviewed found an association between a genetic variant and lower risk of contracting covid-19; another large-scale study, focused on couples in which one person got sick while the other didn’t, kicked off in Oct. 2021.
“My speculation is that something will be borne out there, because it has been well observed that resistance embedded in genetic variation is selected in pandemics,” Pullen says. But most experts suspect that even if they are able to identify such a variant with some certainty, it’s likely to be rare. For now, it’s best for those who haven’t gotten covid to assume they’re as susceptible as anyone else. Whatever the reasons some people haven’t yet gotten sick, the best defense remains staying up to date with vaccinations and avoiding contact with the virus.
“Being exposed to the SARS-CoV-2 virus doesn’t always result in infection, and we’ve been keen to understand why,” study author Rhia Kundu said in a statement, using the scientific name for the coronavirus. “We found that high levels of pre-existing T cells, created by the body when infected with other human coronaviruses like the common cold, can protect against COVID-19 infection.”
The study, which examined 52 people who lived with someone who contracted the coronavirus, found that those who didn’t get infected had significantly higher levels of T cells from previous common cold coronavirus infections. T cells are part of the immune system and believed to protect the body from infection. “Our study provides the clearest evidence to date that T cells induced by common cold coronaviruses play a protective role against SARS-CoV-2 infection,” study author Ajit Lalvani said in a statement.
Researchers cautioned that the findings should not be relied upon as a protection strategy. “While this is an important discovery, it is only one form of protection, and I would stress that no one should rely on this alone,” Kundu said. “Instead, the best way to protect yourself against COVID-19 is to be fully vaccinated, including getting your booster dose.” And the findings on the subject have been inconsistent, with other studies actually suggesting that previous infection with some coronaviruses have the opposite effect.
A major question that has come from the so-called ‘never COVID’ group is whether genetics plays a role in preventing infection. In fact, the question has spurred a team of international researchers to look for people who are genetically resistant to COVID-19 in the hopes that their findings could improve therapeutics. “What we are doing essentially is that we are testing the hypothesis that some people might not be able to get infected because of their genetic and inborn makeup, meaning that they might be genetically resistant to COVID,” says Spaan, who is a member of the COVID Human Genetic Effort.
The effort has sequenced genetic data from about 700 individuals so far, but enrollment is ongoing and researchers have received thousands of inquiries, according to Spaan. The study has several criteria, including laboratory test confirmation that the person has not had previous COVID-19 infection, intense exposure to the virus without access to personal protective equipment like masks and an unvaccinated status at the time of exposure, among others. So far, the group doesn’t know what the genetic difference could be – or if it even exists at all, though they believe it does.
“We do not know how frequent it is actually occurring,” Spaan says. “Is it like a super rare individual with a very, very rare mutation? Or is that something more common?” But the hypothesis is “embedded in human history,” according to Spaan. “COVID is not quite the first pandemic that we are dealing with,” Spaan says. “Humans have been exposed to viruses and other pathogens across time from the early beginning, and these infections have left an imprint on our genetic makeup.”
Those who haven’t gotten the coronavirus are “very much at risk,” says Murphy of Northwestern University. “I think every unvaccinated person is going to get it before this is over.” Experts stressed that research to determine why some people get COVID-19 while others don’t is still very much underway, and no one should rely on any of the hypotheses for protection. Instead, those who haven’t gotten the coronavirus should continue mitigation measures that have been proven to work, like vaccination and mask-wearing.
“You don’t ever want to have COVID,” Murphy says. “You just don’t know which people are going to get really sick from this and die or who’s going to get long COVID, which is hard to diagnose and difficult to treat and very real.” But with coronavirus cases on the rise and mitigation measures like mask mandates dropping left and right, it’s not an easy task.
The following is a summary of some recent studies on COVID-19. They include research that warrants further study to corroborate the findings and that has yet to be certified by peer review.
Fourth vaccine dose protects vs Omicron for at least a month
A fourth dose of the COVID-19 vaccine from Pfizer and BioNTech provided significant added protection against severe disease, hospitalization and death for at least a month in older individuals, according to a study conducted when the Omicron variant was dominant.
The estimated effectiveness of the fourth dose during days 7 to 30 after it was administered compared with a third dose given at least fourth months earlier was 45% against infection, 55% for symptomatic disease, 68% for hospitalization, 62% for severe disease and 74% for death, the research team reported on Wednesday in The New England Journal of Medicine.
The study compared 182,122 individuals aged 60 and older who received a fourth dose and 182,122 very similar people who had received a third dose but not a fourth.
“The results of our real-world study suggest that a fourth vaccine dose is, at least initially, effective against the Omicron variant,” the researchers said. “Additional follow-up will allow further assessment of the protection provided by the fourth dose over time.”
A recently published study that looked only at rates of breakthrough infections and serious illness after the fourth dose found that efficacy waned quickly versus infection but held steady versus severe illness.
COVID-19 may increase risk for rare eye clots. Patients with COVID-19 may have an increased risk of rare vision-threatening blood clots in the eye for months afterward, new findings suggest.
Because SARS-CoV-2 infections increase the risk of blood vessel obstructions at other sites in the body, researchers studied nearly half a million COVID-19 patients to see whether they would develop clots in the veins or arteries of the retina, the nerve tissue at the back of the eye that receives images and sends them to the brain.
Over the next six months, 65 patients had a retinal vein occlusion. While that number is low, it reflects a statistically significant 54% increase compared with pre-COVID infection rates, according to a report published on Thursday in JAMA Ophthalmology.
Retinal artery clots were 35% more common after COVID-19 than before, but that difference might have been due to chance. The clots most often occurred in patients with other conditions that increased their risk of blood vessel problems, such as diabetes, high blood pressure, and high cholesterol.
Compared with a third vaccine dose, a fourth dose of the Pfizer/BioNTech COVID-19 vaccine lowered the risk of infection, symptomatic infection, hospitalization, severe illness, and death 52% to 76%—depending on the measure—amid the Omicron surge among older adults.
Protection against infection waned, however, after 5 weeks, but not protection against severe COVID-19. The findings were published yesterday in the New England Journal of Medicine.
Seven to 30 days after the fourth COVID-19 dose, vaccine effectiveness (VE) relative to the third dose was estimated at 45% against infection (95% confidence interval [CI], 44% to 47%), 55% against symptomatic illness (95% CI, 53% to 58%), 68% against COVID-19 hospitalization (95% CI, 59% to 74%), 62% against severe disease (95% CI, 50% to 74%), and 74% against death (95% CI, 50% to 90%).
Fourteen to 30 days after the fourth dose, VE was 52% (95% CI, 49% to 54%) against infection, 61% (95% CI, 58% to 64%) against symptomatic illness, 72% (95% CI, 63% to 79%) against hospitalization, 64% (95% CI, 48% to 77%) against severe disease, and 76% (95% CI, 48% to 91%) against death.
In the fourth week after the fourth dose, the adjusted infection rate was lower by a factor of 2.0 (95% CI, 1.9 to 2.1) than that in the three-dose group and lower by a factor of 1.8 (95% CI, 1.7 to 1.9) than that among controls.
The difference in absolute risk for COVID-19 hospitalization 7 to 30 days after a fourth vaccine dose, relative to a third, was 180.1 per 100,000 people (95% CI, 142.8 to 211.9), while it was 68.8 cases per 100,000 (95% CI, 48.5 to 91.9) for severe disease. A sensitivity analyses of VE against infection had similar results as those in the primary analysis.
Starting in the fifth week after the fourth dose, the rate ratio (RR) for infection began to fall. The adjusted rate of infection in the eighth week after the fourth dose was comparable to that of internal controls. The RR for the three-dose group relative to the four-dose group was 1.1, while the rate ratio for the internal control group, compared with the four-dose groups, was 1.0.
The RRs comparing controls with fourth-dose recipients were larger and lasted longer for severe disease. In the fourth week after the fourth dose, the adjusted rate of severe disease was lower by a factor of 3.5 than in three-dose recipients and a factor of 2.3 than in internal controls.
The adjusted rate of severe illness in the fourth week after the fourth dose was 1.6 cases per 100,000 person-days, compared with 5.5 cases per 100,000 in three-dose recipients and 3.6 cases per 100,000 in internal controls. The adjusted rate differences were 3.9 fewer cases per 100,000 person-days and 2.1 fewer cases per 100,000 than the three-dose group and internal controls, respectively.
Sick Woman Lying In Bed With Tissues (Getty Images/Obradovic)
