4.6 Article

SARS-CoV-2 Variant of Concern 202012/01 Has about Twofold Replicative Advantage and Acquires Concerning Mutations

Journal

VIRUSES-BASEL
Volume 13, Issue 3, Pages -

Publisher

MDPI
DOI: 10.3390/v13030392

Keywords

COVID-19 pandemic; SARS-CoV-2; spike protein; VOC-202012; 01; spike L18F; genome sequencing; mutation

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Funding

  1. Norwegian Financial Mechanism GRIEG-1 grant [2019/34/H/NZ6/00699]

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The novel SARS-CoV-2 Variant of Concern (VOC)-202012/01, known as B.1.1.7, first identified in the UK in September 2020, has rapidly spread globally and is of concern due to its potential impact on vaccine effectiveness. The VOC has acquired significant mutations, including some that may compromise the binding of neutralizing antibodies, and it is essential to monitor its molecular evolution to understand its impact on the ongoing pandemic.
The novel SARS-CoV-2 Variant of Concern (VOC)-202012/01 (also known as B.1.1.7), first collected in United Kingdom on 20 September 2020, is a rapidly growing lineage that in January 2021 constituted 86% of all SARS-CoV-2 genomes sequenced in England. The VOC has been detected in 40 out of 46 countries that reported at least 50 genomes in January 2021. We have estimated that the replicative advantage of the VOC is in the range 1.83-2.18 [95% CI: 1.71-2.40] with respect to the 20A.EU1 variant that dominated in England in November 2020, and in range 1.65-1.72 [95% CI: 1.46-2.04] in Wales, Scotland, Denmark, and USA. As the VOC strain will likely spread globally towards fixation, it is important to monitor its molecular evolution. We have estimated growth rates of expanding mutations acquired by the VOC lineage to find that the L18F substitution in spike has initiated a fast growing VOC substrain. The L18F substitution is of significance because it has been found to compromise binding of neutralizing antibodies. Of concern are immune escape mutations acquired by the VOC: E484K, F490S, S494P (in the receptor binding motif of spike) and Q677H, Q675H (in the proximity of the polybasic cleavage site at the S1/S2 boundary). These mutants may hinder efficiency of existing vaccines and expand in response to the increasing after-infection or vaccine-induced seroprevalence.

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