Increased infectivity, antibody escape drive SARS-CoV-2 evolution,
studies say
Date:
February 16, 2022
Source:
American Chemical Society
Summary:
Researchers report that omicron and other SARS-CoV-2 variants are
evolving increased infectivity and antibody escape, according to
an artificial intelligence (AI) model. Therefore, new vaccines
and antibody therapies are desperately needed, the researchers say.
FULL STORY ========================================================================== First announced by the World Health Organization on Nov. 26, 2021, the
SARS- CoV-2 omicron variant spread rapidly around the world, becoming
the dominant variant in the U.S. and elsewhere. Now, researchers report
in ACS Infectious Diseasesand the Journal of Chemical Information
and Modeling that omicron and other variants are evolving increased
infectivity and antibody escape, according to an artificial intelligence
(AI) model. Therefore, new vaccines and antibody therapies are desperately needed, the researchers say.
========================================================================== Understanding how SARS-CoV-2 evolves is essential to predicting vaccine breakthrough and designing mutation-proof vaccines and monoclonal
antibody treatments. In a recent study in ACS Infectious Diseases,
Guo-Wei Wei and colleagues analyzed almost 1.5 million SARS-CoV-2
genome sequences taken from people with COVID-19. They identified 683
unique mutations in the receptor binding domain (RBD), the region of
the SARS-CoV-2 spike protein that attaches to the human ACE2 receptor
on the surface of human cells. Then, they used an AI model to predict
how these mutations affect binding strength of the RBD to ACE2 and to
130 antibody structures, including several monoclonal antibodies used
as therapies. The team found that mutations to strengthen infectivity
are the driving force for viral evolution, whereas in highly vaccinated populations, mutations that allow the virus to escape vaccines become
dominant. The researchers also predicted that certain combinations of
mutations have a high likelihood of massive spread.
In another study in the Journal of Chemical Information and Modeling, Wei
and colleagues took a deep dive into the omicron variant's infectivity,
vaccine breakthrough and antibody resistance. They used their AI model
to analyze how the variant's unusually high number of mutations on the
spike protein affect RBD binding to ACE2 and antibodies. Their results indicated that omicron is over 10 times more infectious than the original coronavirus and 2.8 times more infectious than the delta variant. In
addition, omicron is 14 times more likely than delta to escape current vaccines, and it is predicted to compromise the efficacy of several
monoclonal antibody therapies. Many of these predictions have been
verified by emerging experimental results, stressing the importance of developing a new generation of vaccines and monoclonal antibodies that
won't be easily affected by viral mutations, the researchers say.
The authors acknowledge funding from the National Institutes of Health,
the National Science Foundation, NASA, the Michigan Economic Development Corporation, the Michigan State University Foundation, Bristol-Myers
Squibb and Pfizer.
========================================================================== Story Source: Materials provided by American_Chemical_Society. Note:
Content may be edited for style and length.
========================================================================== Journal References:
1. Rui Wang, Jiahui Chen, Yuta Hozumi, Changchuan Yin, Guo-Wei
Wei. Emerging
Vaccine-Breakthrough SARS-CoV-2 Variants. ACS Infectious Diseases,
2022; DOI: 10.1021/acsinfecdis.1c00557
2. Jiahui Chen, Rui Wang, Nancy Benovich Gilby, Guo-Wei Wei. Omicron
Variant
(B.1.1.529): Infectivity, Vaccine Breakthrough, and Antibody
Resistance.
Journal of Chemical Information and Modeling, 2022; 62 (2): 412
DOI: 10.1021/acs.jcim.1c01451 ==========================================================================
Link to news story:
https://www.sciencedaily.com/releases/2022/02/220216082952.htm
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