This has led to speculation about whether a population can achieve some sort of immunity against the virus with only 20% infection – a proportion well below the widely accepted collective immunity threshold (60 to 70% ).
The Swedish public health authority announced in late April that the capital, Stockholm, “was showing signs of collective immunity”, believing that about half of its population had been infected. However, the authority had to go back two weeks later, when the results of its own antibody study revealed that only 7.3% had been infected. But the number of deaths and infections in Stockholm is falling rather than increasing – despite the fact that Sweden has not imposed a lock.
The hope that the COVID-19 pandemic could end sooner than feared has been fueled by speculation about “immunological dark matter”, a type of preexisting immunity that cannot be detected with testing. of SARS-CoV-2 antibodies.
Antibodies are produced by B cells in the body in response to a specific virus. Dark matter, however, involves a characteristic of the innate immune system called “T-cell mediated immunity”. T cells are produced by the thymus gland and when they meet molecules that fight viruses, called antigens, they become programmed to fight the same or similar viruses in the future.
Studies show that people infected with SARS-CoV-2 do indeed have T cells programmed to fight this virus. Surprisingly, people who have never been infected also harbor protective T cells, possibly because they have been exposed to other coronaviruses. This can lead to a certain level of protection against the virus – which could explain why some epidemics seem to die out well below the expected herd immunity threshold.
Young people and people with mild infections are more likely to have a T-cell response than older people – we know that the pool of programmable T cells decreases with age.
In many countries and regions that have experienced very few COVID-19 cases, hot spots are now emerging. Take Germany, which has fought the virus quickly and effectively and has one of the lowest mortality rates among the large countries of northern Europe.
Here, the R number – reflecting the average transmission rate – increased again, below 1 until June 18, but climbed to 2.88 a few days later, and dropped back a few days later. It may be tempting to argue that this could be due to the fact that hot spots have never been close to the 20% infection seen in other regions.
But there are counterexamples, although particularly in elderly and immunocompromised populations. In the Italian epicenter COVID-19 in Bergamo, a city where one in four residents is retired, 60% of the population had antibodies in early June.
The same is true in some prisons: at the Trousdale Turner correctional center in Hartsville, in the United States, 54% of inmates had tested positive for COVID-19 in early May. And more than half of the residents of some long-term care facilities have also been infected.
Genes and the environment
So how do you explain this? Could people living in places with higher levels of positive antibodies have a different genetic makeup?
At the start of the pandemic, there was a lot of speculation as to whether specific genetic receptors affected susceptibility to the SARS-CoV-2 virus. Geneticists thought that variation in DNA ACE2 and TMPRSS2 genes can affect the sensitivity and severity of the infection. But studies to date have shown no convincing evidence to support this hypothesis.
Early reports from China also suggested that blood groups could play a role, with blood group A increasing the risk. This was recently confirmed in studies on Spanish and Italian patients, who also discovered a new genetic risk marker called “3p21.31”.
While genetics can be important, the environment is also important. It is well known that airborne droplet transmission is improved in colder climates. Super-spread events at several meat production facilities where the indoor climate is cold suggests that this has increased contagion. People also tend to spend more time indoors and nearby in bad weather.
The warm weather, however, brings people together, albeit outside. Indeed, June was unusually hot and sunny in many northern European countries, causing parks and beaches to be overtaken and non-compliance with social distancing rules. This will likely cause contagion and cause further outbreaks of COVID-19 in the coming weeks.
Yet another factor is how interpersonal interactions affect contagion. Some previous models assumed that people interact in the same way regardless of their age, well-being, social status, etc. But this is unlikely to be the case – young people, for example, probably have more knowledge than older people. Taking this into account reduces the herd’s immunity threshold to around 40%.
Will COVID-19 disappear?
Large-scale bans, combined with responsible actions by many citizens, have undoubtedly mitigated the spread of SARS-CoV-2 and saved lives. Indeed, in cases like Sweden – where foreclosure has been avoided and social distancing rules have been relatively relaxed – the virus has claimed more lives than its pro-locking neighbors, Norway and Finland.
But blockages alone are unlikely to explain the fact that infections fell in many areas after 20% of the population was infected – which, after all, happened in Stockholm and the cruise ships.
That said, the fact that more than 20% of people have been infected in other places means that the T-cell hypothesis is unlikely to be the only explanation. Indeed, if there is a 20% threshold, it only applies to certain communities, depending on the interactions between many genetic, immunological, behavioral and environmental factors, as well as the prevalence of pre-existing diseases.
Understanding these complex interactions will be necessary to significantly estimate when SARS-CoV-2 will die. Attributing apparent public health successes or failures to a single factor is attractive – but it is unlikely to provide sufficient insight into how COVID-19, or anything to come, can be overcome .