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Reduced levels of convalescent neutralizing antibodies against SARS-CoV-2 B.1+L249S+E484K lineage

Autores participantes:

https://www.medrxiv.org/content/10.1101/2021.09.13.21263430v1

Diego Alejandro Alvarez Diaz, Katherine Laiton Donato, Orlando Alfredo Torres Garcia, Hector Alejandro Ruiz Moreno, Carlos E Franco Munoz, Maria Angie Beltran, Marcela Mercado Reyes, Dra. Ana Luisa MuñozDr. Miguel Germán Rueda

This article is a preprint and has not been certified by peer review [what does this mean?]. It reports new medical research that has yet to be evaluated and so should not be used to guide clinical practice.

The E484K mutation at the SARS-CoV-2 Spike protein emerged independently in different variants around the world, probably as part of the ongoing adaptation of the virus to the human host, and has been widely associated with immune escape from neutralizing antibodies generated during previous infection or vaccination.

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In this work, the B.1+L249S+E484K lineage was isolated along with A.1, B.1.420 and B.1.111 SARS-CoV-2 lineages without the E484K mutation and the neutralizing titer of convalescent sera was compared using microneutralization assays.

While no significant differences in the neutralizing antibody titers were found between A1 and B lineages without the E484K mutation, the neutralizing titers against B.1+L249S+E484K were 1.5, 1.9, 2.1, and 1.3-fold lower than against A.1, B.1.420, B.1.111-I, and B.1.111-II, respectively. However, molecular epidemiological data indicate that there is no increase in the transmissibility rate associated with this new lineage. Hence, although the evidence provided in this study support a Variant of Interest Status (VOI) for the B1+L249S+E484K lineage, enhanced laboratory characterization of this particular lineage and other emerging lineages with the E484K mutation should be carried out in individuals with immunity acquired by natural infection and vaccination.

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This study accentuated the capability of new variants with the E484K mutation to be resistant to neutralization by humoral immunity, and therefore the need to intensify surveillance programs.

Funding Statement

This work was supported by funds from the Fundación Banco Nacional de Sangre Hemolife (CEMIN-10-2020) and the Instituto Nacional de Salud, Bogota D.C, Colombia (CORHUCO project).

For more details on Authors and Declarations go to: https://www.medrxiv.org/content/10.1101/2021.09.13.21263430v1

Fundación Banco Nacional de Sangre Hemolife

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