(1) Via “masgramondou” a must-read perspective article in the British Medical Journal by associate editor Peter Doshi
Read the whole thing (it’s open access), but just a few highlights:
Even in local areas that have experienced some of the greatest rises in excess deaths during the covid-19 pandemic, serological surveys since the peak indicate that at most only around a fifth of people have antibodies to SARS-CoV-2: 23% in New York, 18% in London, 11% in Madrid.123 Among the general population the numbers are substantially lower, with many national surveys reporting in single digits[…] Yet a stream of studies that have documented SARS-CoV-2 reactive T cells in people without exposure to the virus are raising questions about just how new the pandemic virus really is, with many implications.
In a study of donor blood specimens obtained in the US between 2015 and 2018, 50% displayed various forms of T cell reactivity to SARS-CoV-2.511 A similar study that used specimens from the Netherlands reported T cell reactivity in two of 10 people who had not been exposed to the virus.7
In Germany reactive T cells were detected in a third of SARS-CoV-2 seronegative healthy donors (23 of 68). In Singapore a team analysed specimens taken from people with no contact or personal history of SARS or covid-19; 12 of 26 specimens taken before July 2019 showed reactivity to SARS-CoV-2, as did seven of 11 from people who were seronegative against the virus.8 Reactivity was also discovered in the UK and Sweden.
In fact, the article points out, “we’ve been in this movie before”
SWINE FLU DEJA VU. In late 2009, months after the World Health Organization declared the H1N1 “swine flu” virus to be a global pandemic, Alessandro Sette was part of a team working to explain why the so called “novel” virus did not seem to be causing more severe infections than seasonal flu.12
Their answer was pre-existing immunological responses in the adult population: B cells and, in particular, T cells, which “are known to blunt disease severity.”12 Other studies came to the same conclusion: people with pre-existing reactive T cells had less severe H1N1 disease.1314 In addition, a study carried out during the 2009 outbreak by the US Centers for Disease Control and Prevention reported that 33% of people over 60 years old had cross reactive antibodies to the 2009 H1N1 virus, leading the CDC to conclude that “some degree of pre-existing immunity” to the new H1N1 strains existed, especially among adults over age 60.15
The data forced a change in views at WHO and CDC, from an assumption before 2009 that most people “will have no immunity to the pandemic virus”16 to one that acknowledged that “the vulnerability of a population to a pandemic virus is related in part to the level of pre-existing immunity to the virus.”17 But by 2020 it seems that lesson had been forgotten.
Furthermore, Doshi goes into recent studies that reconsider the herd immunity threshold from a mathematical point of view
Nearly 50 years later, Gabriela Gomes, an infectious disease modeller at the University of Strathclyde, is reviving concerns that the theory’s basic assumptions [behind the common first-order herd immunity estimate] do not hold. Not only do people not mix randomly, infections (and subsequent immunity) do not happen randomly either, her team says. “More susceptible and more connected individuals have a higher propensity to be infected and thus are likely to become immune earlier. Due to this selective immunization by natural infection, heterogeneous populations require less infections to cross their herd immunity threshold,” they wrote.22 While most experts have taken the R0 for SARS-CoV-2 (generally estimated to be between 2 and 3) and concluded that at least 50% of people need to be immune before herd immunity is reached, Gomes and colleagues calculate the threshold at 10% to 20%.2223
(2) If the latter is so — and if you keep in mind that documented COVID19 infections are just the tip of the iceberg, with 90% of more beneath the surface — then these graphs from Sweden make some sense. (H/t: Yves not-Cohen)
Swedish public health chief Anders Tegnell, when criticized about the Swedish “Sonderweg” (special road; road alone), said “ask me again in another year”. With 88,000 documented infections out of a population of 10.23 million, they still seem far away from herd immunity — but if you assume a 10:1 to 20:1 Dunkelziffer, and if you also assume a sizable chunk of the population already has some cross-reactivity from common cold coronaviruses, then the virus may simply “be running out of easy targets”.