UC Berkeley Public Health Clinical Professor Emeritus John Swartzberg is one of the nation’s leading authorities on infectious diseases and vaccinology—and an eloquent commentator on all things pathogenic, including the novel coronavirus. California caught up with him recently to get his views on the likely directions of the SARS-CoV-2 pandemic, the prospects for a vaccine, and the American response to date.
This conversation has been edited for length and clarity.
What do you think are probable scenarios for the pandemic as we move towards the end of the year?
John Swartzberg: I’m optimistic by nature, but I’m having a lot of trouble maintaining that optimism as I look ahead to late fall and winter. The United States has 4 percent of the world’s population—and 20 percent of the SARS-CoV-2 infections and 22 percent of the deaths. By any metric, that’s a terrible performance, especially for the wealthiest nation on earth.
We locked down when the pandemic started, but then we loosened up in May. By June, we had 20,000 cases a day. But we continued to loosen strictures through most of June, and we had a tremendous surge in July and August—I think we all remember those incredibly disturbing photos of people crowded together at the Lake of the Ozarks. So by August we hit a zenith of 70,000 cases daily. And we tightened down again, and things started moving in the right direction because people were behaving more appropriately.
But now, we’re in another upswing. People are fatigued emotionally, and that’s a major component in the resistance that’s developed. Currently, we’re seeing about 60,000 cases a day. So we’ve tripled the June daily infection baseline from 20,000, and we’re heading into fall and winter, and that makes me very concerned. We know this virus does very well during these seasons. As the weather becomes cooler, people concentrate indoors, and that vastly increases the risk of transmissibility. We’re also likely to have more children and young adults back in school by late winter, which also exacerbates risk.
Also, we’re going to have to deal simultaneously with influenza, which typically starts in late October and peaks January through February. If we have a bad or even an average influenza season on top of the SARS-CoV-2 pandemic, the nation’s public health system could be overwhelmed. On a positive note, the Southern Hemisphere [which recently saw the end of its winter] had a very mild influenza season. In fact, it set records for the low number of cases, possibly due to the use of personal protective measures and social distancing, which work well for influenza viruses as well as SARS-CoV-2. So maybe we’ll have a similar experience.
The Trump administration seems to be pursuing a de facto policy of “herd immunity” as a pandemic response. What are your views on that?
JS: It’s extremely misguided. They’re basing it on the assumption that if enough people become infected and develop immunity there’s not enough places for the virus to go, and it eventually dies out. So let’s do a back-of-the-envelope calculation: So far, about 10 percent of the U.S. population has been infected, with a death toll of 218,000. We still have a lot to learn about this virus, but most [experts] think you’re going to need about 60 percent of the population infected before you’d achieve anything approaching herd immunity. So extrapolating mortality rates to date, we’re looking at 1.5 million deaths to achieve herd immunity. And those deaths are just the tip of the iceberg. For every person who dies, many, many more are hospitalized, and many of those end up in the ICU. And of those who become seriously ill, many—including some young people—will be ‘long haulers,’ who suffer brain, heart or lung damage, or experience chronic fatigue. Further, we also have to consider the great number of people who may eventually recover, but who suffer terribly because of this disease. When health experts discuss ‘herd immunity,’ it has always been within the context of vaccination. No authority in the history of public health has ever advocated letting people get sick. It’s simply inimical to accepted public health policy.
And finally, we don’t know how long people will stay immune from a natural infection. All we can say for sure at this point is that it could last nine months [the length of the pandemic through September]. We know from other coronaviruses—SARS [CoV-1], MERS, the four coronaviruses that cause the common cold—that there is no demonstrable case for permanent immunity. For the common cold, for example, immunity ranges from one to two years. So sacrificing 1.5 million people for ‘herd immunity’ that is not permanent—that would have to be repeated every one or two years—is a horrible idea. It’s perverted thinking, and it’s incredibly sad that some very well-educated people are promoting it.
Where are we with vaccines in terms of development, approval, and distribution? Also, do we have any sense of probable efficacy?
JS: The very earliest we should expect an approved vaccine would be late November or December. My best guess is we’ll see approvals sometime during the first quarter of 2021. And more than one vaccine may be approved. But even after approval, distribution will take a long time. My best guess here is that it would take about nine months from approval—or about this time next year—to get everyone vaccinated. Or rather, to get everyone vaccinated who wants to be vaccinated. Many people are likely to decline because they don’t trust the President, the FDA or the CDC. And it breaks my heart to say this, but I understand their hesitation. I implicitly trust the people who work at the FDA and CDC, but the agencies are now so politicized that you can’t trust their pronouncements. Personally, I won’t roll up my sleeve until the National Academy of Medicine, the Infectious Disease Society of America, trustworthy independent agencies, and independent universities and scientists all look at the data and give their imprimatur.
Will vaccines alone be sufficient to stem the pandemic?
JS: That gets back to efficacy. The FDA will approve a vaccine that is 50 percent efficacious. For comparison, ‘effective’ flu vaccines are usually around 50 to 60 percent efficacious. But let’s be generous, and say a SARS-CoV-2 vaccine is developed that is 70 percent effective. And everyone gets to review the data, no one is dropping dead, and there’s widespread public acceptance. So about 80 percent of the population—a pretty high figure—gets the vaccine. That leaves 20 percent of the population unvaccinated. And with a vaccine that’s 70 percent effective, you still have maybe 24 percent of the vaccinated population vulnerable to infection. So even with an ‘effective’ vaccine and a good vaccination rate, you end up with 44 percent of the population that is not immune. And many of those people are likely to be asymptomatic, and continue spreading the virus. That’s a major problem, and it’s the reason I’ll still wear a mask and practice social distancing even after vaccines are approved and distributed.
What is the difficulty in developing vaccines with greater efficacy rates?
JS: The only vaccines that would be dramatic game-changers are sterilizing vaccines, such as those developed for measles and polio. They can provide immunity in about 95 percent of the cases. If you get a measles vaccination, the virus won’t even grow in your body—forever. But remember, the human immune system doesn’t respond in an ideal fashion to coronaviruses. They have unique characteristics that are problematic, and permanent immunity is elusive. That’s why you have to get influenza shots annually, and it’s why we don’t have vaccines for common colds. Maybe we’ll fare better with SARS-CoV-2, but it’s unlikely.
What are the implications of SARS-CoV-2 mutating?
JS: SARS-CoV-2 appears to mutate relatively slowly, on average about two mutations per month. This is fortunate for us, in that it suggests vaccines may not become obsolete quickly. The D614G mutation may allow the virus to infect cells with greater alacrity, but it does not appear to increase the damage it directly or indirectly causes to our bodies.
How encouraged should we be about the therapeutics that are being developed for the virus?
JS: There’s a lot of enthusiasm, and rightfully so, for monoclonal antibodies. President Trump received a polyclonal antibody treatment for his infection—basically a combination of two monoclonal antibodies. There’s a 100-year precedent behind such treatment, based on the convalescent plasma approach [the process of using antibody-containing blood plasma from recovered patients to help people who are ill]. Monoclonal antibodies are better than just convalescent plasma, because there’s a lot of junk besides antibodies in plasma. The good news is that it’s a therapy that tends to work in most cases if given early. The bad news is that it’s unlikely to work if given late in the progression of the disease. It’s also logistically difficult to administer at a mass scale. Right now, monoclonal antibodies are expensive and must be administered by IV. We don’t have a low-price, intramuscular solution yet, and that’s what could have a broad impact. Ideally, it you suddenly found that you couldn’t smell anything, you had a slight cough and a low-grade fever, you’d be able to get treated quickly with monoclonal antibodies. That’s the kind of thing that could make a real difference at scale.
What about the antiviral medication Remdesivir and other therapeutics?
JS: Remdesivir is struggling. Three studies have been done, and it’s never been shown to prevent death. Some research has shown that it reduces hospital stays, which is significant and worthwhile—but other research found it didn’t reduce hospital stays. It’s an antiviral agent that stops the virus from reproducing, but to work well it has to be administered early, just like with monoclonal antibodies. And again, it must be administered intravenously, so it’s difficult to scale. There is one trial underway utilizing an inhalable solution, and I really want to see the data on that. It would be wonderful if there was an effective nasal spray you could pick up at the pharmacy when you first notice some symptoms, and I’d like to be hopeful, but it frankly feels like a long shot. So in terms of the role Remdesivir will play in treating SARS-CoV-2, my feet are planted firmly in the air.
There are some other things in the pipeline, including Dexamethasone. It’s a corticosteroid that reduces inflammation and immune response [excessive immune response can be fatal in SARS-CoV-2 patients]. But it reduces those effects—and mortality—only for patients who are very ill and oxygen dependent. They’re having to use an oxygen mask or cannula, or they’re on a ventilator. If they’re not gravely sick, Dexamethasone isn’t helpful at all.
Back to President Trump: How would you characterize his response to the pandemic?
JS: Trump and his followers have been perhaps the biggest problem in terms of response. I say this without malice, but with fact. Woodrow Wilson never uttered the word ‘influenza’ during the 1918 epidemic, and I wish Trump had followed that lead, because everything he has said has been so destructive. Trump’s behavior—lying, denigrating science, politicizing the CDC and the FDA, discouraging mask-wearing and social distancing, his attacks on Dr. [Anthony] Fauci—has cost the lives of thousands of Americans. His political rallies are classic superspreading events that have led to uncounted infections, hospitalizations, and deaths. He has blood on his hands from about 50 percent of the Americans who have died from SARS-CoV-2.