Corona mutation: a changing virus

It is widely believed that the epidemic is caused by the influenza virus, but researchers working with Marc Van Ranst of Leuven University in Belgium have a different theory. They believe that the pandemic was caused by the abbreviated pathogen HCoV-OC43. HCoV-OC43 is a coronavirus.

Genetic studies have suggested that the pathogen had previously jumped from cattle to humans-like SARS-CoV-2 today-has caused a health crisis. Interestingly, HCoV-OC43 still exists today as one of the seven possible coronaviruses that can infect humans. But the killer was tame: lately, the virus only causes a mild cold.

Does the same thing happen for SARS-CoV-2?

For the next six months, the new coronavirus has taken the world hostage. Officially, more than 8 million people are or have been infected, and the virus has already killed more than 500,000 people. Virologists, epidemiologists and hygienists are doing their best to control the situation. However, they are also learning that SARS-CoV-2 is an unpredictable opponent.

The consequences of the crisis depend not only on the development of medicines and vaccines, but also on how SARS-CoV-2 is biologically transformed in the coming months and years.

The first signs suggest that the virus may continue to adapt to humans. This is good news. Over time, the virus tends to get along well with the host, as a relatively peaceful relationship favors the pathogen. Viruses that kill a smaller number of people are more likely to spread. But things are different.

“In principle, evolution is unpredictable. I’m cautiously optimistic about the reduced risk of SARS-CoV-2,” said Christian Drosten, a virologist at Charite Hospital in Berlin. But I’m not sure.”

It is here

François Balloux, a microbiologist at University College in London, is also studying the characteristics and genetics of the new coronavirus. “It will take a few years, a minimum of 10 years,” he says, “then the virus will probably look as serious as the seasonal flu.” He can be sure, “The virus is ours. With it, we will not remove SARS-CoV-2 anymore.”

The new coronavirus has been around for a short time, but it is already one of the best analyzed pathogens in history. Researchers have decoded over 50,000 genomic sequences and uploaded them to a global databank called GISAID (Global Initiative for Sharing All Influenza Data). With the help of this gene sequence, experts are investigating what points of the pathogen may be vulnerable to drugs and vaccines. They are also investigating how SARS-CoV-2 is changing and how the virus spreads.

Since 2015, Biozentrum physicist Richard Richard at the University of Basel and American biologist Trevor Bedford have sought to better understand the course of the epidemic. Experts have been tracking influenza, deer, and ebola viruses for many years using an online application called Nextstrain (Nextstrain.org). Since January 2020, data researchers are also investigating SARS-CoV-2.

Neher’s software on the computer turns chaotic real-time data into a colorful pathogen family tree. The first SARS-CoV-2 genome dates back to December 2019 and to Wuhan, the central city of China (where SARS-CoV-2 first appeared). From there, the family tree branches into hundreds of branches, each marking one or more mutations in the pathogen’s genome. “Most of them are not important, so they do not affect the infectivity or aggression of the virus. But mutations give us clues as to how the virus spreads.”

Thanks to their tree, Neher and his colleagues, for example, can see that SARS-CoV-2 was introduced from Asia to Europe by various routes in January and February. In Germany, the sequence of early cases in North Rhine-Westphalia in western Germany resembles the Dutch, Austrian, and Belgian samples, but differs from other German cases.

On average, experts record two mutations per month on each branch of the viral family tree. Most of them are so-called silent mutations that do not affect the properties of the virus. But some stand out. And that is of interest to researchers.

Spike problem

Nere moves the mouse onto a branch near the root of the virus phylogenetic tree. An information box called “D614G” will appear on the screen. This is an abbreviation for mutation event, which is currently being intensively discussed among experts.

D614G describes changes in viral S proteins or spikes. It is a club-like attachment that allows the SARS-CoV-2 virus to dock with human cells. A team of researchers led by Bette Korber of the Los Alamos National Laboratory say the mutation occurred in early February and then spread in a “warning” manner. Scientists suspect that mutations give the virus the advantage of evolutionary “fitness” compared to Wuhan’s original virus type. Researchers at the Scripps Institute in Florida confirmed this assessment. In the D614G mutant virus, the number of spikes is “4-5 times” higher than other variants – an ideal prerequisite for faster replication.

Does that mean that SARS-CoV-2 is even more infectious than it is now? There is still uncertainty. The success of a particular variant of a virus does not necessarily have anything to do with its genetic makeup. In the case of SARS-CoV-2, other factors could be just as important, such as blockade measures, international air routes, or just coincidence. Therefore, researchers warn that it is too early to draw lines from small genetic mutations to changes in viral infectivity or disease course.

Researchers from Hangzhou, China, took notice after reporting that some variants of SARS-CoV-2 were 270 times more reproducible than other laboratories. But Drosten is skeptical. “At present, this study says nothing,” he said, arguing that the publication had technical flaws.

Not enough time to change

Similarly, much debate has focused on the team’s study of the origin of the virus under the leadership of Michael Forster of the University of Kiel, Germany. Geneticists have identified three different types of SAR-CoV-2 viruses. The differences between the types could be the result of “complex founder scenarios,” the researchers said. Another explanation could be that Wuhan’s predominant type was “immunologically or environmentally adapted to most of the East Asian population.” The method used in the study, and in the same journal, criticized “some serious flaws.”

The reason for skepticism is simple. SARs-CoV-2 did not have enough time to make a big change. Although coronaviruses are constantly mutated, they have unique repair mechanisms to eradicate harmful mutations.