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The United States and Britain are the two major mutation hotbeds at the moment, according to a non-peer-review paper by Chinese scientists posted on Photo: Bloomberg

Coronavirus may be here for much longer – due to rapid mutations

  • Since January, the virus has gone through at least six major gene changes that boosted its ability to infect and evade the human immune system
  • The US and Britain are the two major virus mutation hotbeds at the moment, say scientists
The novel coronavirus has gone through rapid mutations and may spread for a longer time than expected, according to a joint study by two top epidemic research institutes in China.

Since January, the virus has gone through at least six major changes in its genes that boosted infectivity and “immune escape” – its ability to escape the detection and attack by the human immune system, the researchers found. Most of these mutated strains occurred in America and Europe, they said.

Covid-19, the disease caused by the coronavirus, was likely to “spread much longer than we expected”, said researchers from the State Key Laboratory of Respiratory Disease in Guangzhou and the Shanghai Public Health Clinical Centre in a non-peer-reviewed paper posted on the preprint platform on Tuesday.

The coronavirus uses the spike protein to infect human cells. The spike protein binds with a molecule called angiotensin-converting enzyme 2 (ACE2) in host cells.

Professors Qiu Tianyi and Leng Qibin identified three mutations that improved the binding strength.

One change in the N439K gene, for instance, added a chemical bond between the ACE2 and the spike protein. The three other mutations targeted the immune system.

One of them could destroy an ionic bond between the virus and an antibody that is supposed to neutralise Sars-CoV-2, the official name of the coronavirus.

These mutations were in a way similar to those that occurred in human immunodeficiency virus (HIV) and influenza, which dodge immune attack with fast mutation.

“This means that even if the effective vaccine could be developed for current circulating Sars-CoV-2, the rapid, immune escape trend mutations will cause the [ineffectiveness of the vaccine] in a short time,” Qiu and Leng said.

“Thus, we may expect the vaccine development [to] become a cyclical work … just like the case of influenza virus.”

The United States and Britain are the two major mutation hotbeds at the moment, according to the study. In these countries, thousands of changes have occurred in each of the genes affecting the virus' infectivity and immune escape. 

Some previous studies had found that an average adult had a “cold” caused by other coronaviruses every two years.

The human immune response could have learned from these earlier infections and imposed a selective pressure on some common genes that drove the rapid evolution of Sars-CoV-2, according to the Chinese researchers.

An earlier study by American scientists estimated the pandemic would end next year if humans could establish long-lasting immunity against the virus.

But if the immunity was short-lived, the outbreak would return every year, said the researchers led by Professor Marc Lipsitch from the Harvard TH Chan School of Public Health in a paper published in Science magazine last month.

A research team in Wuhan reported on Tuesday they failed to find long-lasting antibodies among medical workers exposed to the virus at the early stage of outbreak.