Americans need to be prepared, and leaders need to restore their credibility.
I want to get back to the pandemic, which is not at the moment being seen for what it is. It is taking place within a very different context. It has been subsumed by the Upheaval, the culture-shaking event we are undergoing as a nation.
States have begun to reopen, people are going out. Covid-19 feels like yesterday’s story—we don’t want to think about it, we’re barely out of the house. But it’s tomorrow’s story too.
The first wave is still here. It never went away. We have every reason to think another, newer, possibly different wave will come in the late fall (different in that the strain could be more lethal, or less).
We have to keep this in mind and have a plan. Public officials especially should be thinking about one.
Outbreaks continue. Some 800 Americans a day are still dying. The number of new cases in Arizona, California, Florida, Tennessee and Texas is up. Alaska, Kentucky, Mississippi, New Mexico, North Carolina, Puerto Rico and South Carolina are also experiencing increases. Angela Dunn, Utah’s state epidemiologist, said last week that the state’s “sharp spike in cases,” is “not explained easily by a single outbreak or increase in testing. This is a statewide trend.”
Nationally there have been more than two million confirmed cases. The true number of cases may be higher for many reasons, including that, as the Journal reported this week, some testing sites were shut down during protests. Reported deaths are approaching 115,000. The head of the Centers for Disease Control and Prevention, Robert Redfield, told Congress that the demonstrations may turn out to have been “a seeding event.”
It had been assumed the summer would offer a respite, and that seems likely in many places, maybe most. New York, hard hit early on, is experiencing a decline in cases. Coronavirus doesn’t like sunlight, fresh air or warm temperatures. It prefers coolness and poor ventilation in enclosed places, meatpacking plants being the most famous example.
Flus and colds tend to recede in the summer and return in the fall and winter. The 1918 influenza epidemic hit America hard in the spring, but its second, deadlier wave came in October.
Harvard epidemiologist Marc Lipsitchtold the Journal of the American Medical Association that he thinks warmer weather is likely to reduce transmission rates by about 20%: “That’s only enough to slow it down, but not enough to stop it.”
Anthony Fauci can be distressingly deft when speaking on issues that touch on the political, but one never doubts he’s being forthcoming when he speaks of disease. This week he told a biotech conference that Covid-19 has been his “worst nightmare”—a highly infectious new virus that typically attacks the respiratory system, with no clear treatment and no cure. “In a period of four months it has devastated the world,” he said. “And it isn’t over yet.”
Among its mysteries: Why such a case-to-case range of severity? Do the infected who become seriously ill fully recover? Are there “long-term durable effects”? And the illness is “shining a bright light on something we’ve known for a very long time,” Dr. Fauci said, which speaks of the greater vulnerability to and harder impacts on African-Americans and other people of color. It has been a “double whammy” for black people.
“Oh my goodness,” he said, “Where is it going to end?”
Markets often tell you how bright investors are viewing the future. CNBC reported Thursday that “the so-called stay-at-home trade” stocks “bucked the market’s overall negative trend . . . amid growing concerns of a potential second wave of new coronavirus cases.” Netflix and Amazon were up, and so was Zoom Video Communications.
Obviously a vaccine would change everything. Dr. Fauci told Yahoo Finance that “it is very difficult to predict” when and how success will come, but he is, as always, “cautiously optimistic” there might be an answer by the end of this year or the beginning of 2021. Yet “there is no guarantee at all that we are going to have a safe and effective vaccine.”
It is not unhelpful in life generally, at least in historical matters, to expect the worst. You’ll never feel disappointed. If the worst happens your bleak worldview is ratified. If it doesn’t you’re pleasantly surprised.
If you expect the worst on coronavirus you’ll think personal caution and carefulness are absolutely essential this summer, and a hard time is coming late this fall and winter.
Which gets us to the governors, who again will be galvanized.
They were right to take strong action early on in the crisis. There is no doubt that the lockdowns saved many, many lives and allowed hospitals to hold their ground. Some governors moved late, some made big blunders, such as in the New York nursing-home disaster. But at the beginning of the crisis, in the face of federal dithering and denials, they were at least doing something.
Then they got carried away. They received too much adulation, enjoyed the role of savior too much, and the lockdowns became longer. Told we were grateful someone was taking responsibility, they became micromanagers of human life. Briefings became self-aggrandizing and Castroesque in length.
If a big fall wave comes it will arrive in a very different context. The shocked and cooperative citizens of March are the battered, skeptical citizens of June. They saw the inevitable politicization of the process. They saw the illogic and apparent capriciousness of many regulations. They suffered financially and saw little sympathy for their plight. They were lectured and hectored. There was no governmental modesty in it.
There will be exactly zero appetite this fall for daily news conferences in which governors announce the phased, Stage 2 openings of certain sectors that meet certain metrics that some midlevel health-department guy seems to have pulled out of his ear. That was the past three months.
What’s the plan if things turn difficult? People won’t want and may not accept a second lockdown, even in the face of a more lethal iteration of the virus. They will likely in a crisis accept increased calls for voluntary social distancing, mask directives, bans on big events, not that we have big events. But—what else?
The governors gained great stature and authority in March and April and began to lose it in May, as did some in the medical and scientific establishments, who became inconsistent in their advice regarding safety and crowds. What early on seemed nonideological came, inevitably, to look like activism.
But we’re going to need all of them again in the fall. They can turn now to where they started—speaking forcefully of the latest, most reliable facts, of how to save lives, of what history tells us about our predicament. Trouble is coming in the fall, and the country is going to need advice, and to trust the advice-givers.
We are only in Act I. Act II is coming. That’s usually the point in the drama when the deepest complications ensue, and demand resolution.
Of the many things we miss from our pre-pandemic lives, hugging may top the list. We asked scientists who study airborne viruses to teach us the safest way to hug.
A Canadian woman was so desperate to hug her mother during quarantine that she created a “hug glove” using a clear tarp with sleeves so the women could hug through the plastic. A video of two young cousins in Kentucky hugging and weeping after weeks apart in quarantine was shared thousands of times.
“We did not expect for them to react the way they did,” said Amber Collins, who recorded the reunion of her 8-year-old son, Huckston, with his cousin Rosalind Arnett, age 10. “They were so overjoyed they didn’t know how to express themselves, except to cry. This hug shows how powerful the human touch truly is.”
Not only do we miss hugs, we need them. Physical affection reduces stress by calming our sympathetic nervous system, which during times of worry releases damaging stress hormones into our bodies. In one series of studies, just holding hands with a loved one reduced the distress of an electric shock.
“Humans have brain pathways that are specifically dedicated to detecting affectionate touch,” says Johannes Eichstaedt, a computational social scientist and psychology professor at Stanford University. “Affectionate touch is how our biological systems communicate to one another that we are safe, that we are loved, and that we are not alone.”
To learn the safest way to hug during a viral outbreak, I asked Linsey Marr, an aerosol scientist at Virginia Tech and one of the world’s leading experts on airborne disease transmission, about the risk of viral exposure during a hug. Based on mathematical models from a Hong Kong study that shows how respiratory viruses travel during close contact, Dr. Marr calculated that the risk of exposure during a brief hug can be surprisingly low — even if you hugged a person who didn’t know they were infected and happened to cough.
Here’s why. We don’t know the exact dose required for the new coronavirus to make you sick, but estimates range from 200 to 1,000 copies of the virus. An average cough might carry anywhere from 5,000 to 10,000 viruses, but most of the splatter lands on the ground or nearby surfaces. When people are in close contact, typically only about 2 percent of the liquid in the cough — or about 100 to 200 viruses — would be inhaled by or splashed on a person nearby. But only 1 percent of those stray particles — just one or two viruses — actually will be infectious.
“We don’t know how many infectious viruses it takes to make you sick — probably more than one,” said Dr. Marr. “If you don’t talk or cough while hugging, the risk should be very low.”
There’s tremendous variability in how much virus a person sheds, so the safest thing is to avoid hugs. But if you need a hug, take precautions. Wear a mask. Hug outdoors. Try to avoid touching the other person’s body or clothes with your face and your mask. Don’t hug someone who is coughing or has other symptoms.
And remember that some hugs are riskier than others. Point your faces in opposite directions — the position of your face matters most. Don’t talk or cough while you’re hugging. And do it quickly. Approach each other and briefly embrace. When you are done, don’t linger. Back away quickly so you don’t breathe into each other’s faces. Wash your hands afterward.
And try not to cry. Tears and runny noses increase risk for coming into contact with more fluids that contain the virus.
While some of the precautions may sound like a lot of effort for a simple hug, people need options given that the pandemic will be with us for a while, said Julia Marcus, an infectious disease epidemiologist and assistant professor at Harvard Medical School.
“There’s a real challenge right now for older people who worry that they won’t be able to touch or connect with family for the rest of their lives,” said Dr. Marcus. “Keeping hugs brief is particularly important because the risk of transmission increases with more prolonged contact.”
Here are the Dos and Don’ts of hugging, based on the advice of Dr. Marr and other experts.
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DON’T hug face-to-face
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“This position is higher risk because the faces are so close together,” said Dr. Marr. “When the shorter person looks up, their exhaled breath, because of its warmth and buoyancy, travels up into the taller person’s breathing zone. If the taller person is looking down, there is opportunity for the huggers’ exhaled and inhaled breaths to mingle.”
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DON’T hug cheeks together, facing the same direction
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This position, with both huggers looking in the same direction, also is higher risk because each person’s exhaled breath is in the other person’s breathing zone.
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DO hug facing opposite directions
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For a safe, full-body hug, turn your faces in opposite directions, which prevents you from directly breathing each other’s exhaled particles. Wear a mask.
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DO let children hug you around the knees or waist
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Hugging at knee or waist level lowers risk for direct exposure to droplets and aerosols because faces are far apart. There is potential for the child’s face and mask to contaminate the adult’s clothing. So you might consider changing clothes, and wash your hands after a visit that includes hugs. The adult also should look away so as not to breathe down on the child.
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DO kiss your grandchild on the back of the head
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In this scenario, the grandparent is minimally exposed to the child’s exhaled breath. The child could be exposed to the taller person’s breath, so kiss through a mask.
Julian Tang, a virologist and associate professor at the University of Leicester in England who studies how respiratory viruses travel through the air, said he would add one more precaution to a pandemic hug: Hold your breath.
“Most hugs last less than 10 seconds, so people should be able to manage this,” Dr. Tang said. “Then back away to at least two meter separation before talking again to allow them to catch their breath at a safe distance. Holding your breath stops you exhaling any virus into their breathing zone, if you are unknowingly infected — and stops you inhaling any virus from them, if they are unknowingly infected.”
Yuguo Li, a University of Hong Kong engineering professor and senior author on the paper that Dr. Marr cited to make the calculations, said that hugs probably pose less risk than a longer face-to-face conversation. “The exposure time is short, unlike conversation, which can be as long as we like,” he said. “But no cheek kissing.”
Dr. Li said the risk of viral exposure may be highest at the start of the hug, when two people approach each other and could breathe on each other, and at the end, when they pull apart. Wearing a mask is important, as is hand washing, because there’s a low risk of picking up the virus from another person’s hands, skin or clothes.
Dr. Marr noted that because the risk of a quick hug with precautions is very low but not zero, people should choose their hugs wisely.
“I would hug close friends, but I would skip more casual hugs,” Dr. Marr said. “I would take the Marie Kondo approach — the hug has to spark joy.”
Many of the infection’s bizarre symptoms have one thing in common
April, blood clots emerged as one of the many mysterious symptoms attributed to Covid-19, a disease that had initially been thought to largely affect the lungs in the form of pneumonia. Quickly after came reports of young people dying due to coronavirus-related strokes. Next it was Covid toes — painful red or purple digits.
What do all of these symptoms have in common? An impairment in blood circulation. Add in the fact that 40% of deaths from Covid-19 are related to cardiovascular complications, and the disease starts to look like a vascular infection instead of a purely respiratory one.
Months into the pandemic, there is now a growing body of evidence to support the theory that the novel coronavirus can infect blood vessels, which could explain not only the high prevalence of blood clots, strokes, and heart attacks, but also provide an answer for the diverse set of head-to-toe symptoms that have emerged.
“All these Covid-associated complications were a mystery. We see blood clotting, we see kidney damage, we see inflammation of the heart, we see stroke, we see encephalitis [swelling of the brain],” says William Li, MD, president of the Angiogenesis Foundation. “A whole myriad of seemingly unconnected phenomena that you do not normally see with SARS or H1N1 or, frankly, most infectious diseases.”
“If you start to put all of the data together that’s emerging, it turns out that this virus is probably a vasculotropic virus, meaning that it affects the [blood vessels],” says Mandeep Mehra, MD, medical director of the Brigham and Women’s Hospital Heart and Vascular Center.
In a paper published in April in the scientific journal The Lancet, Mehra and a team of scientists discovered that the SARS-CoV-2 virus can infect the endothelial cells that line the inside of blood vessels. Endothelial cells protect the cardiovascular system, and they release proteins that influence everything from blood clotting to the immune response. In the paper, the scientists showed damage to endothelial cells in the lungs, heart, kidneys, liver, and intestines in people with Covid-19.
“The concept that’s emerging is that this is not a respiratory illness alone, this is a respiratory illness to start with, but it is actually a vascular illness that kills people through its involvement of the vasculature,” says Mehra.
A respiratory virus infecting blood cells and circulating through the body is virtually unheard of.
A one-of-a-kind respiratory virus
SARS-CoV-2 is thought to enter the body through ACE2 receptors present on the surface of cells that line the respiratory tract in the nose and throat. Once in the lungs, the virus appears to move from the alveoli, the air sacs in the lung, into the blood vessels, which are also rich in ACE2 receptors.
“[The virus] enters the lung, it destroys the lung tissue, and people start coughing. The destruction of the lung tissue breaks open some blood vessels,” Mehra explains. “Then it starts to infect endothelial cell after endothelial cell, creates a local immune response, and inflames the endothelium.”
A respiratory virus infecting blood cells and circulating through the body is virtually unheard of. Influenza viruses like H1N1 are not known to do this, and the original SARS virus, a sister coronavirus to the current infection, did not spread past the lung. Other types of viruses, such as Ebola or Dengue, can damage endothelial cells, but they are very different from viruses that typically infect the lungs.
Benhur Lee, MD, a professor of microbiology at the Icahn School of Medicine at Mount Sinai, says the difference between SARS and SARS-CoV-2 likely stems from an extra protein each of the viruses requires to activate and spread. Although both viruses dock onto cells through ACE2 receptors, another protein is needed to crack open the virus so its genetic material can get into the infected cell. The additional protein the original SARS virus requires is only present in lung tissue, but the protein for SARS-CoV-2 to activate is present in all cells, especially endothelial cells.
“In SARS1, the protein that’s required to cleave it is likely present only in the lung environment, so that’s where it can replicate. To my knowledge, it doesn’t really go systemic,” Lee says. “[SARS-CoV-2] is cleaved by a protein called furin, and that’s a big danger because furin is present in all our cells, it’s ubiquitous.”
Endothelial damage could explain the virus’ weird symptoms
An infection of the blood vessels would explain many of the weird tendencies of the novel coronavirus, like the high rates of blood clots. Endothelial cells help regulate clot formation by sending out proteins that turn the coagulation system on or off. The cells also help ensure that blood flows smoothly and doesn’t get caught on any rough edges on the blood vessel walls.
“The endothelial cell layer is in part responsible for [clot] regulation, it inhibits clot formation through a variety of ways,” says Sanjum Sethi, MD, MPH, an interventional cardiologist at Columbia University Irving Medical Center. “If that’s disrupted, you could see why that may potentially promote clot formation.”
Endothelial damage might account for the high rates of cardiovascular damage and seemingly spontaneous heart attacks in people with Covid-19, too. Damage to endothelial cells causes inflammation in the blood vessels, and that can cause any plaque that’s accumulated to rupture, causing a heart attack. This means anyone who has plaque in their blood vessels that might normally have remained stable or been controlled with medication is suddenly at a much higher risk for a heart attack.
“Inflammation and endothelial dysfunction promote plaque rupture,” Sethi says. “Endothelial dysfunction is linked towards worse heart outcomes, in particular myocardial infarction or heart attack.”
Blood vessel damage could also explain why people with pre-existing conditions like high blood pressure, high cholesterol, diabetes, and heart disease are at a higher risk for severe complications from a virus that’s supposed to just infect the lungs. All of those diseases cause endothelial cell dysfunction, and the additional damage and inflammation in the blood vessels caused by the infection could push them over the edge and cause serious problems.
The theory could even solve the mystery of why ventilation often isn’t enough to help many Covid-19 patients breathe better. Moving air into the lungs, which ventilators help with, is only one part of the equation. The exchange of oxygen and carbon dioxide in the blood is just as important to provide the rest of the body with oxygen, and that process relies on functioning blood vessels in the lungs.
“If you have blood clots within the blood vessels that are required for complete oxygen exchange, even if you’re moving air in and out of the airways, [if] the circulation is blocked, the full benefits of mechanical ventilatory support are somewhat thwarted,” says Li.
A new paper published last week in the New England Journal of Medicine, on which Li is a co-author, found widespread evidence of blood clots and infection in the endothelial cells in the lungs of people who died from Covid-19. This was in stark contrast to people who died from H1N1, who had nine times fewer blood clots in the lungs. Even the structure of the blood vessels was different in the Covid-19 lungs, with many more new branches that likely formed after the original blood vessels were damaged.
“We saw blood clots everywhere,” Li says. “We were observing virus particles filling up the endothelial cell like filling up a gumball machine. The endothelial cell swells and the cell membrane starts to break down, and now you have a layer of injured endothelium.”
Finally, infection of the blood vessels may be how the virus travels through the body and infects other organs — something that’s atypical of respiratory infections.
“Endothelial cells connect the entire circulation [system], 60,000 miles worth of blood vessels throughout our body,” says Li. “Is this one way that Covid-19 can impact the brain, the heart, the Covid toe? Does SARS-CoV-2 traffic itself through the endothelial cells or get into the bloodstream this way? We don’t know the answer to that.”
In another paper that looked at nearly 9,000 people with Covid-19, Mehra showed that the use of statins and ACE inhibitors were linked to higher rates of survival.
If Covid-19 is a vascular disease, the best antiviral therapy might not be antiviral therapy
An alternative theory is that the blood clotting and symptoms in other organs are caused by inflammation in the body due to an over-reactive immune response — the so-called cytokine storm. This inflammatory reaction can occur in other respiratory illnesses and severe cases of pneumonia, which is why the initial reports of blood clots, heart complications, and neurological symptoms didn’t sound the alarm bells. However, the magnitude of the problems seen with Covid-19 appear to go beyond the inflammation experienced in other respiratory infections.
“There is some increased propensity, we think, of clotting happening with these [other] viruses. I think inflammation in general promotes that,” Sethi says. “Is this over and above or unique for SARS-CoV-2, or is that just because [the infection] is just that much more severe? I think those are all really good questions that unfortunately we don’t have the answer to yet.”
Anecdotally, Sethi says the number of requests he received as the director of the pulmonary embolism response team, which deals with blood clots in the lungs, in April 2020 was two to three times the number in April 2019. The question he’s now trying to answer is whether that’s because there were simply more patients at the hospital during that month, the peak of the pandemic, or if Covid-19 patients really do have a higher risk for blood clots.
“I suspect from what we see and what our preliminary data show is that this virus has an additional risk factor for blood clots, but I can’t prove that yet,” Sethi says.
The good news is that if Covid-19 is a vascular disease, there are existing drugs that can help protect against endothelial cell damage. In another New England Journal of Medicine paper that looked at nearly 9,000 people with Covid-19, Mehra showed that the use of statins and ACE inhibitors were linked to higher rates of survival. Statins reduce the risk of heart attacks not only by lowering cholesterol or preventing plaque, they also stabilize existing plaque, meaning they’re less likely to rupture if someone is on the drugs.
“It turns out that both statins and ACE inhibitors are extremely protective on vascular dysfunction,” Mehra says. “Most of their benefit in the continuum of cardiovascular illness — be it high blood pressure, be it stroke, be it heart attack, be it arrhythmia, be it heart failure — in any situation the mechanism by which they protect the cardiovascular system starts with their ability to stabilize the endothelial cells.”
Mehra continues, “What we’re saying is that maybe the best antiviral therapy is not actually an antiviral therapy. The best therapy might actually be a drug that stabilizes the vascular endothelial. We’re building a drastically different concept.”
