Nearly 20,000 Americans have died from COVID-19 over the past seven days. The hypercontagious U.K. variant is rapidly spreading through Florida, while a South African strain infamous for its resilience against antibodies has been spotted in California. Our government’s lackadaisical approach to genomic surveillance leaves us blind to precisely how prevalent these mutants are — and yet, even as other nations have responded to the emergence of such strains with lockdowns, our cities are reopening indoor dining just in time to accelerate their spread. Meanwhile, America’s vaccine rollout remains plagued by logistical difficulties, poor planning, and mass paranoia. As a result, many thousands of Americans are going to die prematurely in the weeks to come.
So, that’s the bad news. Fortunately, the good news is more abundant and heartening than some recent coverage of the pandemic suggests.
The emergence of new, hypervirulent COVID variants has exacerbated the difficulty of reaching herd immunity — the point at which such a high percentage of the population is incapable of transmitting the virus, it gradually dies away. In fact, as my colleague David Wallace-Wells has explained, should the most transmissible strains become dominant, herd immunity against COVID may become a mathematical impossibility. This development has (understandably) attracted much journalistic notice. But headlines lamenting herd immunity’s elusiveness are liable to mislead some lay observers. Eradicating the novel coronavirus may take centuries. But ending the COVID crisis should only take a few more months.
In press accounts, herd immunity is commonly characterized as the “long-promised end of the pandemic.” And it may be true that herd immunity is a precondition for the pandemic’s end in technical terms. But we don’t need to attain such immunity to reach the point at which the novel coronavirus becomes a public-health problem on par with familiar flu or cold strains; which is to say, the point where it poses no threat of severe illness to the vaccinated or challenge to the capacity of any region’s hospital system. If COVID follows the path of previous coronaviruses and becomes an endemic common cold, then we will never reach herd immunity against it. But I don’t think that many of us would describe a world in which you need to get a COVID booster shot every few years — or else face the risk of a mild respiratory illness — to be one where the pandemic never ended.
For most Americans, the primary question is when life will return to some approximation of normality. This is impossible to answer with certainty. Polls suggest that vaccine hesitancy is waning in the U.S., but surveys may underrepresent the socially distrustful segment of the population most likely to spurn vaccination. President Biden announced Thursday that his administration has now purchased enough vaccine doses to inoculate every American adult. But how many bottlenecks will emerge in the distribution process remains unclear. The most menacing source of potential delay, however, has been the prospect that the new COVID variants might prove resistant to the existing vaccines. That is the one hypothetical that threatens to turn our present era into America’s first COVID winter. Happily, newly released studies indicate that this hypothetical is far-fetched.
At least one major vaccine appears to work against all known variants (and will likely work against future mutants too).
This week, virologists at Oxford produced strong evidence that Pfizer’s vaccine promotes a robust immune response against both the British and South African COVID variants. The British research team extracted blood from individuals who had received either one or two doses of the Pfizer mRNA vaccine then introduced isolates of the U.K. (B117) and South African (B1.351) COVID variants into those blood samples and observed how the antibodies and T cells of the vaccinated held up in battle with the COVID mutants.
Among those who’d received a single dose of vaccine, antibodies demonstrated moderate efficacy against the original COVID-19 virus, limited efficacy against the U.K. variant, and virtually none against the South African one.
But the T cells in these samples produced a robust response against all three strains.
What this means: One dose of the Pfizer vaccine will not reliably protect you from being infected with the new COVID variants, but it will likely mitigate the severity of your illness, as your white blood cells will be primed to beat back an invasion by COVID viruses of all stripes.
Meanwhile, 90 percent of those who had received the full two-dose regimen of the Pfizer vaccine produced neutralizing antibodies against all of the variants, meaning that — in the vast majority of cases — the vaccine insulated subjects from the threat of even mild illness, no matter the strain.
The coronavirus is not done evolving, of course. But Oxford’s findings offer strong cause for thinking that the Pfizer vaccine will hold up against emergent variants: Although slight discrepancies between the spike protein of the original coronavirus (which the vaccines are modeled on) and that of the new variants confuse antibodies, T cells appear to develop a broader model of the virus upon exposure to the vaccine, one that allows them to identify a COVID bug for what it is, no matter its idiosyncrasies.
To be sure, one non-peer-reviewed laboratory study should not be taken as the last word on any subject. But over the past few weeks, Israel conducted a real-life test of the Pfizer vaccine’s efficacy against the British variant — and it proved as potent in the nursing homes of Tel Aviv as it had been in the labs of Oxford.
Between January 16 and February 6, the U.K. variant began spreading exponentially through Israel. Over the same period, roughly 3.5 million predominantly older Israelis received the Pfizer vaccine. The shots beat the spread: By February 6, among Israelis 60 or over, cases of COVID had fallen by 53 percent, hospitalizations by 39 percent, and severe illness by 31 percent. Among those infected with British variant specifically, the vaccine demonstrated between 90 and 95 percent efficacy, according to the Israeli Health Ministry.
Notably, in interviews with the Guardian, Oxford’s research team said that they had “confidence” that the other existing vaccines would prove similarly effective against the new strains.
The vaccines should offer substantial protection against transmission.
Beyond fears of novel variants, a separate concern about vaccine efficacy has centered on their impact on transmission. Most vaccines were approved based on their effectiveness in preventing illness in individuals who received them, not on their efficacy in preventing individuals from asymptomatically carrying the virus and then passing it on to another (potentially vulnerable, unvaccinated) person.
But the available evidence suggests that the vaccines should curb transmission significantly. Multiple studies, including a recent analysis of COVID clusters in Spain published in The Lancet, have shown that viral load is a (if not the) critical variable for COVID transmission. The novel coronavirus is both highly infectious and highly dependent on superspreaders to perpetuate itself; most people who contract the virus do not pass it on to anyone else, even their close contacts. The defining, non-behavioral characteristic of superspreaders appears to be the amount of virus in their bodies. In The Lancet study, viral load was more predictive of passing on the virus than symptoms (though these were correlated).
Data from researchers in Israel indicate that the Pfizer vaccine dramatically reduces viral load in those infected with the virus, even if they’ve only taken a single dose. Last week, a preliminary analysis of the Oxford-AstraZeneca vaccine’s impact on transmission showed reductions in viral load large enough to cut the rate of transmission by up to 67 percent.
It’s (almost) the end of the pandemic as we’ve known it.
It is possible that the (figuratively) darkest days of America’s winter are still to come. The ongoing spread of hypercontagious variants, pervasive flouting of public-health guidelines, and logistical headaches afflicting the vaccine rollout could coalesce into a perfect epidemiological storm.
But it seems more likely that the worst of the pandemic is behind us. COVID cases in the U.S. have been plummeting for weeks now, and the decline can no longer be dismissed as a reversion to the preholiday season mean. One theory that is consistent with the data: COVID’s seasonality is driven primarily by sunlight, and thus, as the days began growing longer, the virus began having more difficulty passing between hosts. This hypothesis is consistent with a recent paper in the journal Nature suggesting that the timing of COVID outbreaks last fall correlated less with temperature levels than it did with latitude; where sunlight first dwindled, COVID first began surging.
Whatever the near-term future brings, summer is all but certain to slow the virus’s spread. Given COVID’s seasonality, and the extraordinary caliber of the vaccines, it is well within our power to end the public-health crisis before the days grow dark again. The most plausible obstacle to this outcome may be the persistence of vaccine hesitancy in pockets of our society. It is unclear exactly what persuading the skeptical will require. But downplaying the apparent efficacy of the vaccines — or obscuring how close we are to escaping this era of mass death and social isolation by foregrounding the hard math of herd immunity — probably will not help.
