4.8 Article

Immunological imprinting of the antibody response in COVID-19 patients

Journal

NATURE COMMUNICATIONS
Volume 12, Issue 1, Pages -

Publisher

NATURE PORTFOLIO
DOI: 10.1038/s41467-021-23977-1

Keywords

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Funding

  1. CRIP (Center for Research on Influenza Pathogenesis), a NIAID funded Center of Excellence for Influenza Research and Surveillance (CEIRS) [HHSN272201400008C]
  2. SEM-CIVIC, a NIAID funded Collaborative Influenza Vaccine Innovation Center [75N93019C00051]
  3. NCI SeroNet grant [U54CA260560]
  4. JPB Foundation
  5. Instituto de Salud Carlos III, Spanish Ministry of Science, Innovation and Universities (PFIS contract) [FI18/00183]
  6. JPB Foundation, the Open Philanthropy Project [2020-215611 (5384)]

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The study found that previous infections with seasonal coronaviruses can affect the antibody response to SARS-CoV-2 in COVID-19 patients. While SARS-CoV-2 infection can boost pre-existing responses to other coronaviruses, this back-boosting hampers the induction of specific antibodies against SARS-CoV-2.
In addition to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), humans are also susceptible to six other coronaviruses, for which consecutive exposures to antigenically related and divergent seasonal coronaviruses are frequent. Despite the prevalence of COVID-19 pandemic and ongoing research, the nature of the antibody response against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is unclear. Here we longitudinally profile the early humoral immune response against SARS-CoV-2 in hospitalized coronavirus disease 2019 (COVID-19) patients and quantify levels of pre-existing immunity to OC43, HKU1 and 229E seasonal coronaviruses, and find a strong back-boosting effect to conserved but not variable regions of OC43 and HKU1 betacoronaviruses spike protein. However, such antibody memory boost to human coronaviruses negatively correlates with the induction of IgG and IgM against SARS-CoV-2 spike and nucleocapsid protein. Our findings thus provide evidence of immunological imprinting by previous seasonal coronavirus infections that can potentially modulate the antibody profile to SARS-CoV-2 infection. In addition to SARS-CoV-2, other coronaviruses also infect human, but whether consecutive infections cross-modulate the induced immune response is still unclear. Here the authors show that SARS-CoV-2 infection boosts pre-existing responses to other coronaviruses, yet such back-boosting hampers the induction of specific antibodies against SARS-CoV-2.

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