America is staring down a widespread COVID-19 testing shortage with no vaccine in sight. So what happens when coronavirus makes its unceremonious return?
“There’s a possibility that the assault of the virus on our nation next winter will actually be even more difficult than the one we just went through,” Robert Redfield, director of the Centers of Disease Control and Prevention, told The Washington Post.
“And when I’ve said this to others, they kind of put their head back, they don’t understand what I mean,” Redfield told the paper late Tuesday. “We’re going to have the flu epidemic and the coronavirus epidemic at the same time.”
“ ‘There’s a possibility that the assault of the virus on our nation next winter will actually be even more difficult than the one we just went through.’ ”
Anthony Fauci, the director of the National Institute of Allergy and Infectious Diseases, also said the novel coronavirus “might keep coming back” year after year. “The ultimate game changer in this will be a vaccine,” he said. But that, Fauci estimated, could take 12 to 18 months.
“If we’re not expecting a second wave or a mutation of this virus, then we have learned nothing,” New York Gov. Andrew Cuomo, told CMCSA, +0.05% earlier this month, calling it a “new normal” for public health in the U.S. “That is why it is such an important period for government.”
First, the bad news: “The four seasonal coronaviruses do not seem to induce long-term immunity,” said Gregory Poland, who studies the immunogenetics of vaccine response in adults and children at the Mayo Clinic in Rochester, Minn., and expert with the Infectious Diseases Society of America.
“We will not have a vaccine by next winter,” Poland added. “The Southern Hemisphere is just starting their fall and winter. They will have a severe course of this disease due to less preparedness, less medical infrastructure and less public infrastructure.”
Coronavirus immunity differs from other diseases. Immunizations against smallpox, measles or Hepatitis B should last a lifetime, Poland said. Coronaviruses, first discovered in the 1960s, interact with our immune system in unique and different ways, he added.
How do other coronaviruses compare to SARS-CoV-2? People infected by SARS-CoV, an outbreak that centered in southern China and Hong Kong from 2002 to 2004, had immunity for roughly two years; studies suggest the antibodies disappear six years after the infection.
For MERS-CoV, a coronavirus that has caused hundreds of cases in the Middle East, people retain immunity for approximately 18 months — although the long-term response to being exposed to the virus again may depend on the severity of the original infection.
The world, Poland said, should brace itself for round two: “We will start moving into our summer when they’re moving into their winter,” he said. “If, as is likely, we don’t restrict all travel, cases will start coming back into the Northern Hemisphere and we’ll have another outbreak this fall.”
It’s too early for ‘herd immunity’ to be effective
Without a vaccine, “herd immunity” is another option. That theory was briefly considered in the U.K. as an alternative to closing businesses and practicing social distancing, but was deemed too risky. Ultimately, enough people would need to be immune to shield the most vulnerable.
“There’s no chance that immunity is going to be high enough to reach herd immunity,” Poland said. “With influenza, you need herd immunity of 60% to 70%. With measles, you need about 95%. With COVID-19, it’s somewhere in the middle.”
In the absence of a vaccine, Poland said several conditions are necessary for herd immunity to work: a very high level of population immunity, for that immunity to be durable, and for the virus to not mutate. “None of those seem to be operational at present,” he said.
“ With influenza, you need herd immunity of 60% to 70%. With measles, you need about 95%. With COVID-19, it’s somewhere in the middle. ”
In addition to the level of herd immunity (or lack thereof) to protect those who are most vulnerable, people will have to be cognizant of the disease spreading through asymptomatic carriers — that is, people who are infected but show no signs that they’re ill.
For example, a New England Journal of Medicine study published this month found that 29 (or 14%) of 210 pregnant women arriving at New York–Presbyterian Allen Hospital and Columbia University Irving Medical Center tested positive for COVID-19, yet displayed no symptoms.
“Our use of universal SARS-CoV-2 testing in all pregnant patients presenting for delivery revealed that at this point in the pandemic in New York City, most of the patients who were positive for SARS-CoV-2 at delivery were asymptomatic,” the study concluded.
“It underscores the risk of Covid-19 among asymptomatic obstetrical patients,” added the study, which was published earlier this month. “Moreover, the true prevalence of infection may be underreported because of false negative results of tests to detect SARS-CoV-2.”
Lessons in immunity from the Spanish flu of 1918
So what will happen if or when SARS-CoV-2, which causes the respiratory disease COVID-19, returns? “We’re just 14 weeks into this, so no one knows,” Poland said. If it has a slight mutation, he added, the response of our antibodies will be “moderately irrelevant.”
We can’t expect to have the same “herd immunity” or “original antigenic sin” — the ability of our immune systems to remember a virus that is similar, but not the same, as a previous version — as influenza. Influenza, after all, has been around for 500, if not 1,000 years.
“During the great influenza pandemic of 1918, the age group that disproportionately died were young people, not older adults,” Poland said. “Older adults had seen previews of this virus in earlier years, probably in the late 1800s, so they had immunological memory.”
“ ‘The 1918 Spanish flu’s second wave was even more devastating than the first wave. COVID-19’s sweet spot could be October to May.’ ”
There are similarities between influenza and SARS-CoV-2, and they have almost identical symptoms — fever, coughing, night sweats, aching bones, tiredness, and nausea and diarrhea in the most severe cases. Like all viruses, neither are treatable with antibiotics.
They can both be spread through respiratory droplets from coughing and sneezing, but they come from two different virus families — and ongoing research to develop a universal vaccine for influenza shows how tricky both influenza viruses and coronaviruses can be.
“The 1918 Spanish flu’s second wave was even more devastating than the first wave,” Ravina Kullar, an infectious-disease expert with the Infectious Diseases Society of America and adjunct faculty member at the University of California, Los Angeles, told MarketWatch.
Historians believe that a more virulent influenza strain hit during a hard three months in 1918 and was spread by troops moving through Europe during the First World War. A mutated strain would be a worst-case scenario for a second wave of SARS-CoV-2 this fall or winter.
The 1918 pandemic is forever associated with Spain, but this strain of H1-N1 was discovered earlier in Germany, France, the U.K. and the U.S., but similar to the Communist Party’s response to first cases of COVID-19 in Wuhan, China, First World War censors buried or underplayed those reports.
”It is essential to consider the deep connections between the Great War and the influenza pandemic not simply as concurrent or consecutive crises, but more deeply intertwined,” historian James Harris wrote in an essay on the pandemic.
“ A more virulent, mutated strain of the novel coronavirus would be a worst-case scenario for a second wave of SARS-CoV-2 this fall or winter. ”
The British military medicine took a leading role in studying the public-health response, he added. “Domestic public-health leaders did almost nothing to stem the spread of the pandemic due to the impact measures such as quarantine would have had on the war effort.
Doctors and members of the public, as of now, were spooked by how otherwise strong, healthy people fell victim to the 1918 influenza. Doctors today attribute that to the “cytokine storm,” a process where the immune system in healthy people reacts so strongly as to hurt the body.
A surge of immune cells and their activating compounds (cytokines) effectively turned the body against itself, led to an inflammation of the lungs, severe respiratory distress, leaving the body vulnerable to secondary bacterial pneumonia.
And the second wave of SARS-CoV-2? “It will likely hit harder in areas not severely impacted the first time in the interior of the U.S., where there’s a lot more susceptible people,” Kullar said. “COVID-19’s sweet spot could be October to May, with it peaking, likely, in October and November.”
Kullar said scientists are learning something new every day from modeling studies. “If it follows the same pattern as influenza, it will likely level off during the summertime,” she said. “If immunity is in existence, then likely the virus will come back looking for new victims.”
What’s more, Redfield told the Washington Post that he’s been in talks with state officials about the potential for using U.S. Census Bureau, Peace Corps and AmeriCorps volunteers to create what he called “an alternative workforce” to help with contact tracing for those who test positive.
Testing will determine the rate of asymptomatic carriers
There is reason to be optimistic. “We still have a lot to learn about the flu, even though we’ve had flu vaccines since the mid-1940s,” Poland said. “It’s amazing what the world has done in 14 weeks on COVID-19, but what’s more amazing is how much more there is to learn.”
In those 14 weeks, scientists around the world have learned a lot about SARS-CoV-2, including the virus’s genetic structure; how it infects human cells; what kind of disease manifestation it causes; and how it impacts the liver, kidney and brain.
“ ‘We really need to have wide-scale testing available, and contact tracing to find everyone who has been exposed.’ ”
What else, aside from social distancing to “flatten the curve” of new infections, can be done between now and then? While scientists work to crack the code of the novel coronavirus, the government and members of the public can work together.
“It all comes down to testing,” Kullar said. “We really need to have wide-scale testing available, and contact tracing to find everyone who has been exposed and get them to self-isolate for 14 days. We don’t have a system like that in the U.S. at present.”
Just over 4.1 million people have been tested in the U.S. for SARS-CoV-2, there are 840,476 confirmed cases, and nearly 46,611 deaths. Testing has been delayed by shortages of reliable tests nationwide. A recent Reuters poll suggested 2.3% were diagnosed with COVID-19.
On Monday, more than 50 days after the first coronavirus case was reported in New York, the state began random antibody testing on consenting grocery-store patrons in different regions across the state. There is no guarantee as yet that the presence of antibodies confers immunity.
The procedure, also known as serology testing, uses a finger-stick blood sample. It will analyze 3,000 people across New York, which has a population of 19.5 million, over the next week, Gov. Andrew Cuomo said on Sunday. But questions remain about the tests’ effectiveness.
Cuomo met with President Trump on Tuesday at the White House and said that the president had offered federal assistance to help New York State carry out up to 40,000 coroanvirus tests a day, which the governor said he hopes will happen within several weeks.
Assuming testing is up to speed by the end of summer, Kullar says Americans should be on a sound footing for round two of SARS-CoV-2 with, ideally, enough hospital supplies and testing in place to ensure we all make fewer mistakes next time around.
But a lot will come down to the American people. “How we behave will really determine how big this virus is going to get,” she said. “Maintain social distancing and wear masks in public until we see infection rates go down, and keep doing it until we get enough testing.”