UPDATE: This story was updated on Aug. 21 to reflect the falling infection fatality rate in England
When Italian Dr. Matteo Bassetti, the head of the infectious diseases clinic at the San Martino hospital in Genoa, suggested back at the end of May that the SARS-CoV-2 virus driving the global pandemic appeared to be mutating toward a weaker strain, he was quickly shouted down in a world where some now seem to want things to be as bad as they can be.
“Experts dispute reports that coronavirus is becoming less lethal,” the Washington Post promptly reported. Other media generally followed along with websites for the medical profession leading the way.
“In stark opposition to Bassetti’s and other doctors’ statements, Italian public health officials and the World Health Organization (WHO) warn there’s no evidence to support these claims,” WebMD reported.
In the weeks that followed, the pandemic news – especially in the U.S. – quickly shifted away from the observations of Bassetti and a few others to the uptick in new cases of COVID-19, the disease caused by the virus, and the politics of masks. The editorial board of the Los Angeles Times even tied the two together to blame the lack of a national mask mandate for the increase in cases although the data linking masks and rates of infection is all over the place.
Cases of COVID-19 peaked in little-masked Sweden in late June and fell all through July before beginning an August uptick that mirrored that of much of the rest of masked Europe, according to q Swedish tracker that incorporates data from the Swedish health agency and John Hopkins University in the U.S.
The potency picture
What is most interesting about the data in Sweden – where the increase in reported infections has been attributed in part to increased testing – is the difference between current infection rates and serious cases of the disease.
Since the beginning of August, Sweden has been reporting 200 to 300 new cases per day. But the death rate of 2.4 to 4.4 cases per day along with the rate of admissions to intensive care units (ICUs) – 1.1 to 2.4 per day – are a fraction of what they were in the spring.
Back in late March with cases in the range of 200 to 300 per day, deaths and ICUs admissions (adjusted for the lag time between diagnosis and outcomes) were in the range of 70 to 90 per day for fatalities and 41 to 44 for ICU admissions.
Or, to put this simply, the disease looked somewhere near 20 times as deadly in late March as it does now. The numbers reflect what the Italians reported they were seeing in May, and the Italians and the Swedes are not alone.
Scientists at the Centre for Evidence-Based Medicine at the University of Oxford in England on Friday reported the infection fatality rate (IFR) in that country fell 55 to 80 per cent in the six weeks between June 23 and Aug. 4.
“Office for National Statistics (ONS) figures imply an IFR as of 4 August estimated at 0.49 per cent,” they said. “The IFR estimate was higher at 2.63 per cent at the start of our eight-week series….”
Meanwhile, Harvard University scientists on Tuesday posted a draft study at MedRxiv reporting a big drop in virulence in Massachusetts “among healthcare workers in one system that applied 23 uniform screening criteria throughout the research period.”
As with all the studies at MedRxiv, which has taken research into real time, this one has not been peer-reviewed, and the sample size for the study is small, but the Harvard researchers observed much of what the Italians and English saw and what the Swedish data reflects.
“Existing evidence shows a decreasing case-fatality rate in the United States,” the Harvard researchers wrote. “However, in relation to virulence, this statistic may be biased by improved clinical acumen as well as increased testing detecting more asymptomatic and paucisymptomatic cases.”
That is why the researchers decided to look at regularly tested healthcare workers. The regular testing removed one variable. The researchers split cases found in this group into two time periods, one before April 15 and one after.
“A total of 166 eligible cases were identified in the study period: 98 early and 68 late,” they said. “There were no significant differences between early and late cases regarding age, sex, race, residential community attack rates, and number of presenting symptoms.
“There were a total of 13 cases with any complications in the database, comprised of 12 early cases and one late case. Ten cases experienced hospitalization or death (9 early vs. 1 late). Three cases underwent intubation or a code (all early cases) and two of these HCWs died.
“Our study provides epidemiologic support for the hypothesis of possible
attenuated (reduced) viral virulence….The current study has several strengths. First, we used uniform screening protocols and testing criteria for all employees throughout the study period, minimizing bias from younger and less symptomatic cases detected as testing became more widespread.”
Secondly, they said, the similar pattern of infections between health care workers and others at work in pubic places during the pandemic makes the study reflective of the real world. But they noted the small sample size and lack of medical histories, which is a problem.
A variety of chronic health conditions have been shown to make people far more susceptible to a difficult or deadly case of COVID-19. Still, the study added to the growing evidence backing the Italian observations of months ago.
On the same day the Harvard scientists posted their study of health care workers, researchers from the Cyprus Institute of Neurology & Genetics and the Cyprus School of Molecular Medicine uploaded a different study at BioRxiv, a companion site to MedRxiv, that looked at the genes of the steadily evolving SARS-CoV-2 virus.
“We highlight two interesting mutations found in genes N (P13L) and ORF3 (Q57H),” they wrote. “The former appears to be significantly associated with decreased deaths and cases per million according to our models, while the latter shows an opposing association with decreased deaths and increased cases per million,” they wrote.
Overall, they noted, the many different strains of SARS-CoV-2 now in circulation around the globe (think pink salmon versus red salmon versus chum salmon versus Chinook salmon, all of them being salmon) are genetically very similar, the virus’s “rapid transmission rate provides ample opportunity for natural selection to act upon a range of viral mutations.”
These mutations can go in all sorts of directions, they added, but “it is known that an ‘efficient’ virus does not result in death for the underlining host. Therefore, the overall high transmission and moderate mortality rates of SARS-CoV-2 are what make this virus pandemic material.”
The efficiency issue is basic evolutionary biology. A virus that kills most of its carriers is doomed because it needs carriers to survive. It’s a simple numbers game.
The common cold, another coronavirus, has survived for centuries by infiltrating the human body and surviving there until it can make the jump from one human to another. This is made easy because the cold makes people sick but does not debilitate them.
They are perfectly capable of wandering around and infecting others. Asymptomatic strains of SARS-CoV-2 would likely enjoy a similar evolutionary advantage and thus might come to outweigh deadlier strains.
“Taking the frequently occurring D614G as an example, it is evident that this mutation is becoming the dominant mutation across populations and its rapid spread denotes a natural selection pressure that shows increased fitness for this mutation,” the researchers observed.
“Fitness” for a virus is defined by an increased rate of transmission, as observed for D614G, but “a successful virus will not…kill its host, so increased contamination rates have to be coupled with decreased deaths rates,” they added. “This is exactly what is observed for the Q57H and P13L mutations, which provide a counterbalance” to deadlier strains of SARS-CoV-2.
There is no given milder strains will triumph over deadlier strains, but that appears the most likely evolutionary outcome.
And then there is the much-discussed theory of “herd immunity,” which basically holds that the spread of an infectious disease stops when enough people become immune to it that it cannot easily move from host to host.
Immunity can come either from the antibodies developed by people who’ve survived an infection or via vaccinations, which basically fool the body into creating antibodies in the belief it has been infected.
The herd-immunity theory emerged from a heated debate among epidemiologists in the early 20th Century.
“This controversy was between those who believed that epidemics terminated because of changes in the properties of the infectious agent (e.g., loss of ‘virulence’)…and those who argued that it reflected the dynamics of
the interaction between susceptible, infected, and immune segments of the population,” Paul E.M. Fine wrote in a 1993 history for Epidemiologic Reviews.
“Each argument was supported by observations and by mathematical reasoning. It was the latter explanation that won the day; and its simple mathematical formulation, the “mass action principle,” which has become a cornerstone of epidemiologic theory, provides one of the simplest logical arguments for indirect protection by herd immunity.”
The scientists arguing for a decline in virulence were at the time hampered by the inability to identify the genes of pathogens. Science has come a long way since then as the scientists on Cyprus illustrate.
The questions now being raised about the shifting virulence of the SARS-CoV-2 virus suggest it might be time to reopen the discussion of “herd immunity” which has itself caused considerable controversy and is likely to cause more.
Dr. Anthony Fauci, the man leading the battle against COVID-19 in the U.S., believes a vaccine, which has yet to be developed and might or might not work, must be administered to most Americans to achieve herd immunity in this country. That idea is not popular with the anti-vaccination crowd.
Meanwhile, rogue epidemiologist Anders Tegnell from Sweden is under fire for appearing to try to allow herd immunity to develop naturally there and last week claiming the steadily declining number of serious cases and deaths from COVID-19 in Sweden can only be explained by the development of some sort of immunity in the population.
“Exactly why this happened at that time and why it was so quick and sudden, is difficult for us to understand,” he told a publication of the British, liberal newspaper chain The Guardian. “But we believe that the increasing number of immune people in the population must have something to do with it.”
He went on to guestimate an immunity rate of “20 percent, 30 percent, maybe even slightly more in some areas” despite antibody tests showing far lower rates of past exposure to SARS-CoV-2.
“It’s very difficult to draw a good sample from the population, because obviously, the level of immunity differs enormously between different age-groups, between different parts of Stockholm and so on, and that’s why when we measure one group we get 4 percent to 5 percent, and when we measure another group they’re up to 25 percent,” Tengell said.
“While Sweden’s steady-as-you-go strategy is starting to look more sensible as Denmark, Norway and Finland see a resurgence in cases,” The Guardian added, “Tegnell said he now doubted if there would ever be a definitive answer over which strategy was best.
“‘It will be very difficult to achieve any kind of really clear-cut answer as to what was right and what was wrong,’ he said. ‘I think we’re talking years into the future before we can get any kind of consensus on how to deal with this in the best possible way.'”
For this heretical comment, he almost immediately came under fire. Business Insider – a German-owned, New York-based online publication said to draw as much traffic as the mainstream Wall Street Journal – basically called Tegnell a liar.
said the virus appears to have become less potent, possibly due to genetic mutations, the Sunday Telegraph reported.