What level of antibody response protects against COVID-19 death?

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In a study of patients with COVID-19 being treated in intensive care units, people who mounted only a low antibody response against the virus faced a higher risk of dying, according to international scientists. They also found that patients with strong antibody responses had low levels of viral RNA in their blood, while those with poor antibody responses had high viral RNA levels and viral proteins in their blood. The authors say the findings could help establish the optimal antibody levels needed for an individual to overcome COVID-19 when critically ill. The study also provided evidence of the importance of antibodies against the spike protein of SARS-CoV-2 - the antibodies induced by vaccination -  to block the virus’ replication, the scientists say.

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From: Wiley

What level of antibody response protects against COVID-19 death?

In a study of patients with COVID-19 being treated in intensive care units, people who mounted only a low antibody response against the SARS-CoV-2 virus faced a higher risk of dying.

The study, which is published in the Journal of Internal Medicine, also found that patients with strong antibody responses against the virus had low levels of viral RNA in their blood. On the contrary, those with poor antibody responses had high viral RNA levels and disseminated viral proteins in the blood.

The results could help establish the optimal antibody levels needed for an individual to overcome COVID-19 when critically ill. The study also provided evidence of the importance of antibodies against the spike protein of SARS-CoV-2 to block the virus’ replication. These are the antibodies that are induced by vaccination.

“Our findings support that treatment with exogenous antibodies in COVID-19 should be personalized, reserving this therapy for those patients with absent or low endogenous antibodies levels”, said co–senior author Jesús F. Bermejo-Martin, MD, PhD, of the Instituto de Investigación Biomédica de Salamanca (IBSAL) & CIBERES, in Spain.

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Journal of Internal Medicine
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Organisation/s: Instituto de Investigación Biomédica de Salamanca, Spain, Universidad de Barcelona, Spain
Funder: This work was supported by awards from the Canadian Institutes of Health Research, (CIHR OV2 – 170357), Research Nova Scotia, Atlantic Genome/Genome Canada, Li-Ka Shing Foundation, Dalhousie Medical Research Foundation (David J. Kelvin), David J. Kelvin is a recipient of the Canada Research Chair in Translational Vaccinology and Inflammation, and the “Subvenciones de concesión directa para proyectos y programas de investigación del virus SARS-CoV2, causante del COVID-19”, FONDO - COVID19, Instituto de Salud Carlos III (COV20/00110, CIBERES, 06/06/0028), (Antoni Torres) and finally by the “Convocatoria extraordinaria y urgente de la Gerencia Regional de Salud de Castilla y León, para la financiación de proyectos de investigación en enfermedad COVID-19” (GRS COVID 53/A/20) (CA). Ana P. Tedim was funded by the Sara Borrell Research Grant CD018/0123 funded by Instituto de Salud Carlos III and co-financed by the European Development Regional Fund (A Way to Achieve Europe programme).
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