The Spanish flu pandemic of 1918 spread the world and claimed tens of millions of lives. However, by 1920, the virus that caused the disease became much less dangerous and eventually “degenerated” into the usual seasonal flu. Some pandemics lasted longer, such as the plague that affected eastern and central Asia in the 1940s, but then reached Europe and killed 30 to 60% of the population in Europe, the Middle East and some Asian regions, according to various estimates. However, seven years after the first outbreak, the black death epidemic also came to an end, with American anthropologist Wendy Orent recalling well-known precedents from history.
In the article, published in the US scientific journal Undark, the expert predicts possible transformations of the Covid-19 agent.
Scientists and historians say that the measured bacterium that caused the “black death” has not lost its virulence (the ability of the pathogen to cause disease and death in the infected organism) over time. The virus that caused the 1918 flu pandemic, on the other hand, became less deadly, and it is very likely that the same thing happened with the H1N1 pathogen in 2009.
Will the coronavirus SARS-CoV-2, which causes Covid-19, follow a similar trajectory? Will it become less deadly? It is not yet possible to provide definite answers – a pandemic lasts less than a year. However, a view of the past can provide clues, the author writes.
The pathogen “does not want” to kill the host
The idea that circulating pathogens become less lethal over time has existed since at least the 19th century. American epidemiologist and veterinarian Theobald Smith was the first to suggest that there was a “delicate balance between the parasite and the host.” The scientist claimed that the pathogen should become less lethal over time because the microorganism is not “interested” in killing its host.
This idea became commonplace and was developed in the 1980s. British biologist Roy Anderson and mathematician Robert May suggested that an infected person is more likely to infect others when he releases large amounts of a pathogen, but this usually happens when he is already seriously ill. Thus, virulence and pathogen transmission are inextricably linked, but the “invader” does not kill too quickly, because if the “host” fails to infect anyone before death, the pathogen will not be able to spread.
The best-known example is the myxoma virus, which was introduced to Australia in 1950 specifically to reduce the number of rabbits. These animals were imported from Europe and, as a result of uncontrolled reproduction, became a real punishment for the country’s agriculture.
In the first year, the virus killed more than 99.8% of infected rabbits. The following year, mortality fell to 90%, but later stabilized at around 25%. There was a “truce”: rabbits developed a genetic ability to resist, and the virus became much less deadly. If the pathogen killed all the rabbits, it would die with them.
The pathogen requires a mobile “vehicle”
According to the theory developed by the American epidemiologist Paul Evaldd, the more deadly the microorganism, the less likely it is to spread quickly.
This is logical: if victims lose their ability to move very quickly after infection (as is the case, for example, with Ebola virus disease), they cannot spread the infection further. If the infection requires a mobile host to spread, its ability to kill will inevitably decline.
Virulence theory recognizes that the ability of many microorganisms to kill will shrink as they spread and adapt to the human population. However, Evald’s theory does not rule out the possibility that different pathogens have different transmission strategies, and in some of them a high ability to infect and a high ability to kill combine.
One such strategy is liveliness. For example, the smallpox virus is very persistent in the external environment, and mortality from this disease is very high – 30%. Evalds calls this strategy “sit and wait”. Some deadly infections are transmitted from diseased hosts by intermediaries who do not become ill themselves, such as fleas, fists, mosquitoes or ticks. Others, such as cholera, are transmitted through water. Third, such as staphylococcal infections in hospitals, are spread by staff. This is exactly what happened in the maternity wards of hospitals in the 19th century, when doctors and nurses transferred the so-called birth fever agents from one mother to another.
According to Evalds, these strategies may slow down the reduction of pathogen virulence.
How will SARS-CoV-2 behave?
But what prediction can these theories make for SARS-CoV-2? What is the likelihood that the virulence of the new coronavirus will decrease as it is transmitted from person to person on a global scale?
The author proposes to compare the new coronavirus with its “relative” SARS, which caused the atypical pneumonia pandemic in 2002-2004. per year. The virus spread in the late stages of infection from people who were already seriously ill. In the end, about eight thousand people were infected, 774 died, and the disease was overcome by strict adherence to the rule of isolating the sick.
SARS-CoV-2, unlike “first SARS”, is transmitted at an early stage of infection. Even asymptomatic carriers release enough virus to infect.
Therefore, it seems unlikely that the evolutionary process of SARS-CoV-2 will follow Anderson and May’s “compromise model” that the virus may become both highly infectious and highly deadly over time.
Paul Evalds believes that the persistence of the virus is important for forecasts. He points out that SARS-CoV-2 particles remain on various surfaces for a few hours to several days, making them as resistant as the flu virus. According to him, also in terms of virulence, SARS-Cov-2 will become similar to seasonal flu, with a typical mortality rate of about 0.1%.
There is currently no assurance that SARS-CoV-2 will follow this path. Even current data on mortality with Covid-19 are uncertain, as differences in testing scales and protocols across countries make it impossible to accurately and completely record global infections.
The original strain in Wuhan was less infectious
However, at least one evolutionary coronavirus change is already being observed by scientists.
A group of biologists from the Losalamos National Laboratory in the United States in July publication described in the journal Cell how the mutated strain of coronavirus identified as D614G appears to replace the original strain first found in Wuhan. Based on laboratory studies, the researchers concluded that the new strain was more infectious than the strain found in Wuhan.
This discovery was criticized, but as time has shown, the new strain is now the most common. “The current pandemic is the D614G strain. Today, it is not possible to take a sample containing [oriģinālais] Wuhan Virus. At the beginning of March, it was a completely different virus, ”says Beta Korbere, the study’s leader. In her view, the fact that the original strain has been almost completely replaced indicates that there has been a selection for greater portability.
According to Evald’s analysis, high portability is often associated with lower virulence. He hopes to see evidence that SARS-CoV-2 is evolving in this direction, that is, becoming more contagious but less lethal.
However, other factors must also be taken into account. First, testing is now more accessible than during the first wave of a pandemic. This means that patients are hospitalized and treated earlier, and this gives them a better chance of survival. Second, experimental treatment methods can increase the survival of hospitalized patients. Thirdly, social exclusion measures are effective and the most vulnerable groups, such as people living in old people’s homes, are now better protected from infection.
Vaccination will end the pandemic, but the virus will be with us for a long time to come
Similar to plague, Covid-19 is a latent infection with a long incubation period. The cane suppresses the early response of the immune system, and people can feel healthy for several days after infection, but the infection has already spread. The same thing happens after getting infected with SARS-CoV-2 – symptoms appear after five to ten days, but sometimes later (or not at all).
This “cunning” way of spreading can reduce the possibility that the new coronavirus will evolve less dangerously to humans – infected asymptomatic people are the ideal “vehicles” to deliver the virus to new “recipients”.
However, according to Vincent Rakaniello, a virologist at Columbia University, even if the coronavirus does not evolve through evolution, its effects on humans will diminish.
“SARS-CoV-2 may become less deadly not because the virus has changed, but because few people will be immune,” he said. Mildly ill children who are re-infected with the virus at an older age will be more likely to cope. The virologist states that the four existing coronaviruses that cause the common acute respiratory infection were also transmitted from humans to animals and were probably quite virulent at first. Now 90% of children become infected with them, but later, when they have grown up, re-infection suffers that simple cold.
Compared to influenza viruses, coronaviruses are more stable and are less likely to evolve, trying to overcome existing immunity. Therefore, according to many experts, the best way to get out of the current maze of pandemics is through safe and effective vaccines.
Vaccination may be required on a regular basis, depending on the recurrence of the coronavirus cycle, but not because the virus is significantly in the mouth, but because the developed immunity will gradually weaken. There will be versions of the virus that will continue to circulate, possibly as a simple cold virus. Occasionally there may be isolated outbreaks with deaths in the unvaccinated. One way or another, this virus has been with us for a long time, if not forever, sums up the anthropologist.