Could it be burning after 20% of a population is infected?

More than half a million people have died from COVID-19 worldwide. It is a great tragedy, but perhaps not on the scale that some initially feared. And finally there are signs that the pandemic is shaking in places, as if its engine is running out of fuel. This has encouraged many governments to give up on blockades and allow daily life to restart, albeit cautiously.

The spread of SARS-CoV-2 has been difficult to predict and understand. On the Diamond Princess cruise ship, for example, where the virus is likely to have spread relatively freely through the cabin air conditioning system, only 20% of passengers and crew were infected. Data from military ships and cities like Stockholm, New York and London also suggest that infections have been around 20%, much lower than previous suggested mathematical models.

This has led to speculation about whether a population can achieve some type of immunity to the virus with as little as 20% infection, a proportion well below the widely accepted herd immunity threshold (60-70%).

The Swedish public health authority announced in late April that the capital city Stockholm was “showing signs of collective immunity”, estimating that about half of its population had been infected. However, the authority had to back down 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 decreasing rather than increasing, despite the fact that Sweden has not imposed a blockade.

Hopes that the COVID-19 pandemic may end earlier than initially feared have been fueled by speculation about “immune dark matter,” a pre-existing type of immunity that cannot be detected by antibody tests against the virus. SARS-CoV-2.

Antibodies are produced by body B cells in response to a specific virus. However, dark matter does involve a feature of the innate immune system called “T-cell mediated immunity.” T cells are produced by the thymus and when they encounter virus-fighting molecules, known as antigens, they are programmed to fight the same or similar viruses in the future.

Studies show that people infected with SARS-CoV-2 have T cells programmed to fight this virus. Surprisingly, never-infected people also harbor protective T cells, probably because they have been exposed to other coronaviruses. This can lead to some level of protection against the virus, which could explain why some outbreaks appear to burn well below the herd’s 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 programmable T cell pool decreases with age.

In many countries and regions that have had very few cases of COVID-19, critical areas are now emerging. Take Germany, which quickly and efficiently fought the virus and has one of the lowest death rates among the large countries of northern Europe.

Here, the R number, reflecting the average transmission rate, has risen again, down from 1 through June 18, but shot up to 2.88 just a few days later, only to drop again a few days later. It may be tempting to argue that this could be because the hotspots never came close to the 20% infection seen in other regions.

But there are opposite examples, although particularly in older, immunocompromised populations. At the Italian epicenter COVID-19 in Bergamo, a city where one in four residents are pensioners, 60% of the population had antibodies in early June.

The same is true in some prisons: at the Trousdale Turner Correctional Center in Hartsville, USA, 54% of inmates had tested positive for COVID-19 in early May. And more than half of residents in some long-term care facilities have also been infected.

Genes and environment

So how do we explain this? Could people in places with higher rates of positive antibodies have a different genetic makeup?

Early in the pandemic, there was much speculation about whether specific genetic receptors affected susceptibility to the SARS-CoV-2 virus. Geneticists thought that the variation of DNA in the ACE2 and TMPRSS2 Genes can affect the susceptibility and severity of infection. But studies so far have shown no convincing evidence to support this hypothesis.

Early reports from China also suggested that blood types may play a role, with an increased risk of blood type. This was recently confirmed in studies of Spanish and Italian patients, who also discovered a new genetic risk marker called “3p21.31”.

While genetics may be important, the environment is also important. It is well known that the transmission of airborne droplets increases in colder climates. Wide-spread events at various meat production facilities where the indoor climate is cold suggest that this has increased contagion. People also tend to spend more time indoors and nearby during inclement weather.

However, the warm weather unites people, albeit outdoors. In fact, June has been unusually hot and sunny in many northern European countries, causing the overflow of parks and beaches and the rules of social distancing have been breached. This will likely trigger the spread and cause new outbreaks of COVID-19 in the coming weeks.

Another factor is how interpersonal interactions affect contagion. Some previous models have assumed that people interact in the same way, regardless of age, well-being, social status, etc. But this is probably not the case: young people, for example, are likely to have more acquaintances than the elderly. Taking this into account lowers the herd’s immunity threshold to around 40%.

Will COVID-19 disappear?

The blockades imposed far and wide, combined with the responsible actions of many citizens, have undoubtedly mitigated the spread of SARS-CoV-2 and saved lives. In fact, in cases like Sweden, where blocking was avoided and social distancing rules were relatively relaxed, the virus has taken an order of magnitude more lives than in its pro-blocking neighbors, Norway and Finland.

But blockages alone are unlikely to explain the fact that infections have declined in many regions after 20% of a population has been infected – something that, after all, happened in Stockholm and on cruise ships. .

That said, the fact that more than 20% of people have been infected elsewhere means that the T-cell hypothesis is unlikely to be the only explanation. In fact, if there is a 20% threshold, it applies only to some communities, depending on the interactions between many genetic, immunological, behavioral and environmental factors, as well as the prevalence of pre-existing diseases.

It will be necessary to understand these complex interactions to significantly estimate when the SARS-CoV-2 will burn. It is attractive to attribute any apparent success or failure in public health to a single factor, but it is unlikely to provide sufficient information on how COVID-19 can be defeated, or what comes next.