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Studies show how the D614G variant outperforms the original SARS-CoV-2 virus

 


Prior to the emergence of new variants of coronavirus, such as the British subspecies B.1.1.7, the SARS-CoV-2 mutant named D614G was already from the original SARS-CoV-2 pathogen that caused the pandemic. It was mutated.

D614G spread rapidly and became the most abundant mutant in the world. This D614G mutation remains in all new mutants. An international team, including Bern researchers, was able to show why the D614G mutant was able to dominate the original SARS-CoV-2 virus in both laboratory and animal models.

Our approach also allows us to more appropriately and quickly characterize new mutations such as the British variant B.1.1.7. “

Volker Thiel, Chief Researcher, Institute of Virology and Immunology, University of Bern

The findings show how the fitness benefits of viral variants can lead to higher infections, which is very important for assessing the risk of new mutants spreading. The first results were previously released and allowed scientific discussion about what is known as a preprint server.The results of the study are now fully public Nature..

The D614G variant has a mutation in a peplomer that makes it easier for the virus to dock in human cells.

David E at the IVI and Centers for Disease Control and Prevention in Atlanta, USA. Researchers in Wentworth’s lab first showed that D614G mutants bind more strongly in human cell cultures from the upper respiratory tract and nose. It also replicates faster than the original virus.

Increased replication of the D614G mutant was also confirmed in vivo in the new mouse model first described in this study. These experiments were also conducted at IVI in the Charaf Benarafa group.

New mutations are clearly dominant

The spread of the SARS-CoV-2 virus can be better studied in other animals than in mice. Hamsters and ferrets are well-established in infection studies and are particularly well-established animal models. To compare the two variants, a mixture of the original version of the SARS-CoV-2 virus and an equal portion of the D614G variant was applied to the nose of each animal under light anesthesia.

One day later, ly infected animals were re-reared with another healthy picket of the same species and evaluated for transmission of two mutants that directly competed with each other. The experiment was repeated with a total of 6 pairs of animals. In virtually all sentinels, the proportion of infected SARS-CoV-2 virus was initially largely dominated by the D614G mutant.

Mutant differentiation was performed using state-of-the-art sequencing and PCR techniques by the Friedrich Loeffler Institute in Greifswald-Inselreams and Martin Beer’s team at the Federal Institute for Animal Health (D). “Our study stands out because we were able to clearly identify the more efficient transmission of the mutated variant compared directly to the original variant,” says Volker Thiel.

Fitness test for further mutations

This approach can also be used to test a single mutation or a particular combination of mutations present in many currently circulating viral variants. IVI relies on a cloning technique developed in Bern a year ago to accurately replicate the SARS-CoV-2 virus in the laboratory. For example, the British virus is known to have more than 14 mutations, not just one, eight of which occur in peplomer.

Therefore, with the help of cloning techniques, any number of mutations in a variant can be reproduced and used to compete with each other in established cell culture and animal models. The results show how a single mutation affects the suitability and transmissibility of new mutants. “Our testing strategy allows us to quickly find out why other newly emerging viral variants have been established,” said Volker Thiel.

A similar research project on infectious pathogens may be undertaken in the future at the newly established Interdisciplinary Center for Infectious Diseases and Immunity (MCIDI) at the University of Bern.

Source:

Journal reference:

Zhou, B. , et al.. (2021) SARS-CoV-2 Spike D614G changes enhance replication and transmission. Nature.. doi.org/10.1038/s41586-021-03361-1..

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